Updated on 2022/05/09

写真a

 
KATO Katsuhiro
 
Organization
Nagoya University Hospital Cardiology Assistant professor of hospital
Title
Assistant professor of hospital
External link

Degree 1

  1. Ph.D ( 2012.7   Nagoya University ) 

Research Areas 1

  1. Life Science / Cardiology

Professional Memberships 3

  1. 日本血管生物医学会   評議員

  2. 日本内科学会

  3. 日本循環器学会

Awards 3

  1. 第6回血管生物医学会若手研究会最優秀賞

    2020.11   第6回血管生物医学会若手研究会   臓器特異的な血管網と血管形成

    加藤勝洋

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    Award type:Award from Japanese society, conference, symposium, etc.  Country:Japan

  2. 名古屋大学医師会奨励賞

    2020.1   名古屋大学医師会  

    加藤勝洋

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    Country:Japan

  3. The 4th NAGOYA Global Retreat Best Poster Presentation

    2012.2  

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    Award type:Award from Japanese society, conference, symposium, etc.  Country:Japan

 

Papers 38

  1. Loss of the transcription factor RBPJ induces disease-promoting properties in brain pericytes. Reviewed International coauthorship International journal

    Rodrigo Diéguez-Hurtado, Katsuhiro Kato, Benedetto Daniele Giaimo, Melina Nieminen-Kelhä, Hendrik Arf, Francesca Ferrante, Marek Bartkuhn, Tobias Zimmermann, M Gabriele Bixel, Hanna M Eilken, Susanne Adams, Tilman Borggrefe, Peter Vajkoczy, Ralf H Adams

    Nature communications   Vol. 10 ( 1 ) page: 2817 - 2817   2019.6

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    Sufficient vascular supply is indispensable for brain development and function, whereas dysfunctional blood vessels are associated with human diseases such as vascular malformations, stroke or neurodegeneration. Pericytes are capillary-associated mesenchymal cells that limit vascular permeability and protect the brain by preserving blood-brain barrier integrity. Loss of pericytes has been linked to neurodegenerative changes in genetically modified mice. Here, we report that postnatal inactivation of the Rbpj gene, encoding the transcription factor RBPJ, leads to alteration of cell identity markers in brain pericytes, increases local TGFβ signalling, and triggers profound changes in endothelial behaviour. These changes, which are not mimicked by pericyte ablation, imperil vascular stability and induce the acquisition of pathological landmarks associated with cerebral cavernous malformations. In adult mice, loss of Rbpj results in bigger stroke lesions upon ischemic insult. We propose that brain pericytes can acquire deleterious properties that actively enhance vascular lesion formation and promote pathogenic processes.

    DOI: 10.1038/s41467-019-10643-w

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  2. Pulmonary pericytes regulate lung morphogenesis. Reviewed International coauthorship International journal

    Kato K, Diéguez-Hurtado R, Park DY, Hong SP, Kato-Azuma S, Adams S, Stehling M, Trappmann B, Wrana JL, Koh GY, Adams RH

    Nature communications   Vol. 9 ( 1 ) page: 2448 - 2448   2018.6

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    Blood vessels are essential for blood circulation but also control organ growth, homeostasis, and regeneration, which has been attributed to the release of paracrine signals by endothelial cells. Endothelial tubules are associated with specialised mesenchymal cells, termed pericytes, which help to maintain vessel wall integrity. Here we identify pericytes as regulators of epithelial and endothelial morphogenesis in postnatal lung. Mice lacking expression of the Hippo pathway components YAP and TAZ in pericytes show defective alveologenesis. Mutant pericytes are present in normal numbers but display strongly reduced expression of hepatocyte growth factor leading to impaired activation of the c-Met receptor, which is expressed by alveolar epithelial cells. YAP and TAZ are also required for expression of angiopoietin-1 by pulmonary pericytes, which also controls hepatocyte growth factor expression and thereby alveologenesis in an autocrine fashion. These findings establish that pericytes have important, organ-specific signalling properties and coordinate the behavior of epithelial and vascular cells during lung morphogenesis.

    DOI: 10.1038/s41467-018-04913-2

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  3. Role of the PAR-3-KIF3 complex in the establishment of neuronal polarity Reviewed

    T Nishimura, K Kato, T Yamaguchi, Y Fukata, S Ohno, K Kaibuchi

    NATURE CELL BIOLOGY   Vol. 6 ( 4 ) page: 328 - 334   2004.4

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    Neurons polarize to form elaborate multiple dendrites and one long axon. The establishment and maintenance of axon/dendrite polarity are fundamentally important for neurons. Recent studies have demonstrated that the polarity complex PAR-3-PAR-6-atypical protein kinase C (aPKC) is involved in polarity determination in many tissues and cells. The function of the PAR-3-PAR-6-aPKC protein complex depends on its subcellular localization in polarized cells. PAR-3 accumulates at the tip of growing axons in cultured rat hippocampal neurons, but the molecular mechanism of this localization remains unknown. Here we identify a direct interaction between PAR-3 and KIF3A, a plus-end-directed microtubule motor protein, and show that aPKC can associate with KIF3A through its interaction with PAR-3. The expression of dominant-negative PAR-3 and KIF3A fragments that disrupt PAR-3-KIF3A binding inhibited the accumulation of PAR-3 and aPKC at the tip of the neurites and abolished neuronal polarity. These results suggest that PAR-3 is transported to the distal tip of the axon by KIF3A and that the proper localization of PAR-3 is required to establish neuronal polarity.

    DOI: 10.1038/ncb1118

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  4. Induction of osteogenesis by bone-targeted Notch activation. Reviewed International coauthorship International journal

    Cong Xu, Van Vuong Dinh, Kai Kruse, Hyun-Woo Jeong, Emma C Watson, Susanne Adams, Frank Berkenfeld, Martin Stehling, Seyed Javad Rasouli, Rui Fan, Rui Chen, Ivan Bedzhov, Qi Chen, Katsuhiro Kato, Mara E Pitulescu, Ralf H Adams

    eLife   Vol. 11   2022.2

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    Declining bone mass is associated with aging and osteoporosis, a disease characterized by progressive weakening of the skeleton and increased fracture incidence. Growth and lifelong homeostasis of bone rely on interactions between different cell types including vascular cells and mesenchymal stromal cells (MSCs). As these interactions involve Notch signaling, we have explored whether treatment with secreted Notch ligand proteins can enhance osteogenesis in adult mice. We show that a bone-targeting, high affinity version of the ligand Delta-like 4, termed Dll4(E12), induces bone formation in male mice without causing adverse effects in other organs, which are known to rely on intact Notch signaling. Due to lower bone surface and thereby reduced retention of Dll4(E12), the same approach failed to promote osteogenesis in female and ovariectomized mice but strongly enhanced trabecular bone formation in combination with parathyroid hormone. Single cell analysis of stromal cells indicates that Dll4(E12) primarily acts on MSCs and has comparably minor effects on osteoblasts, endothelial cells, or chondrocytes. We propose that activation of Notch signaling by bone-targeted fusion proteins might be therapeutically useful and can avoid detrimental effects in Notch-dependent processes in other organs.

    DOI: 10.7554/eLife.60183

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  5. Corticotropin releasing hormone receptor 2 antagonist, RQ-00490721, for the prevention of pressure overload-induced cardiac dysfunction. Reviewed International journal

    Yu Mori, Ayako Tsuchihira, Tatsuya Yoshida, Satoya Yoshida, Akiyoshi Fujiuchi, Masashi Ohmi, Yumi Isogai, Teruhiro Sakaguchi, Shunsuke Eguchi, Takuma Tsuda, Katsuhiro Kato, Koji Ohashi, Noriyuki Ouchi, Hyi-Man Park, Toyoaki Murohara, Mikito Takefuji

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie   Vol. 146   page: 112566 - 112566   2022.2

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    BACKGROUND: G protein-coupled receptors (GPCRs) regulate the pathological and physiological functions of the heart. GPCR antagonists are widely used in the treatment of chronic heart failure. Despite therapeutic advances in the treatments for cardiovascular diseases, heart failure is a major clinical health problem, with significant mortality and morbidity. Corticotropin releasing hormone receptor 2 (CRHR2) is highly expressed in cardiomyocytes, and cardiomyocyte-specific deletion of the genes encoding CRHR2 suppresses pressure overload-induced cardiac dysfunction. This suggests that the negative modulation of CRHR2 may prevent the progression of heart failure. However, there are no systemic drugs against CRHR2. FINDINGS: We developed a novel, oral, small molecule antagonist of CRHR2, RQ-00490721, to investigate the inhibition of CRHR2 as a potential therapeutic approach for the treatment of heart failure. In vitro, RQ-00490721 decreased CRHR2 agonist-induced 3', 5'-cyclic adenosine monophosphate (cAMP) production. In vivo, RQ-00490721 showed sufficient oral absorption and better distribution to peripheral organs than to the central nervous system. Oral administration of RQ-00490721 inhibited the CRHR2 agonist-induced phosphorylation of cAMP-response element binding protein (CREB) in the heart, which regulates a transcription activator involved in heart failure. RQ-00490721 administration was not found to affect basal heart function in mice but protected them from pressure overload-induced cardiac dysfunction. INTERPRETATION: Our results suggest that RQ-00490721 is a promising agent for use in the treatment of chronic heart failure.

    DOI: 10.1016/j.biopha.2021.112566

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  6. LPL/AQP7/GPD2 promotes glycerol metabolism under hypoxia and prevents cardiac dysfunction during ischemia. Reviewed International coauthorship International journal

    Sohta Ishihama, Satoya Yoshida, Tatsuya Yoshida, Yu Mori, Noriyuki Ouchi, Shunsuke Eguchi, Teruhiro Sakaguchi, Takuma Tsuda, Katsuhiro Kato, Yuuki Shimizu, Koji Ohashi, Takahiro Okumura, Yasuko K Bando, Hiroaki Yagyu, Nina Wettschureck, Naoto Kubota, Stefan Offermanns, Takashi Kadowaki, Toyoaki Murohara, Mikito Takefuji

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology   Vol. 35 ( 12 ) page: e22048   2021.12

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    In the heart, fatty acid is a major energy substrate to fuel contraction under aerobic conditions. Ischemia downregulates fatty acid metabolism to adapt to the limited oxygen supply, making glucose the preferred substrate. However, the mechanism underlying the myocardial metabolic shift during ischemia remains unknown. Here, we show that lipoprotein lipase (LPL) expression in cardiomyocytes, a principal enzyme that converts triglycerides to free fatty acids and glycerol, increases during myocardial infarction (MI). Cardiomyocyte-specific LPL deficiency enhanced cardiac dysfunction and apoptosis following MI. Deficiency of aquaporin 7 (AQP7), a glycerol channel in cardiomyocytes, increased the myocardial infarct size and apoptosis in response to ischemia. Ischemic conditions activated glycerol-3-phosphate dehydrogenase 2 (GPD2), which converts glycerol-3-phosphate into dihydroxyacetone phosphate to facilitate adenosine triphosphate (ATP) synthesis from glycerol. Conversely, GPD2 deficiency exacerbated cardiac dysfunction after acute MI. Moreover, cardiomyocyte-specific LPL deficiency suppressed the effectiveness of peroxisome proliferator-activated receptor alpha (PPARα) agonist treatment for MI-induced cardiac dysfunction. These results suggest that LPL/AQP7/GPD2-mediated glycerol metabolism plays an important role in preventing myocardial ischemia-related damage.

    DOI: 10.1096/fj.202100882R

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  7. NFAT5/TonEBP Limits Pulmonary Vascular Resistance in the Hypoxic Lung by Controlling Mitochondrial Reactive Oxygen Species Generation in Arterial Smooth Muscle Cells. Reviewed International coauthorship International journal

    Hebatullah Laban, Sophia Siegmund, Maren Zappe, Felix A Trogisch, Jörg Heineke, Carolina De La Torre, Beate Fisslthaler, Caroline Arnold, Jonathan Lauryn, Michael Büttner, Carolin Mogler, Katsuhiro Kato, Ralf H Adams, Hanna Kuk, Andreas Fischer, Markus Hecker, Wolfgang M Kuebler, Thomas Korff

    Cells   Vol. 10 ( 12 )   2021.11

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    Chronic hypoxia increases the resistance of pulmonary arteries by stimulating their contraction and augmenting their coverage by smooth muscle cells (SMCs). While these responses require adjustment of the vascular SMC transcriptome, regulatory elements are not well defined in this context. Here, we explored the functional role of the transcription factor nuclear factor of activated T-cells 5 (NFAT5/TonEBP) in the hypoxic lung. Regulatory functions of NFAT5 were investigated in cultured artery SMCs and lungs from control (Nfat5fl/fl) and SMC-specific Nfat5-deficient (Nfat5(SMC)-/-) mice. Exposure to hypoxia promoted the expression of genes associated with metabolism and mitochondrial oxidative phosphorylation (OXPHOS) in Nfat5(SMC)-/- versus Nfat5fl/fl lungs. In vitro, hypoxia-exposed Nfat5-deficient pulmonary artery SMCs elevated the level of OXPHOS-related transcripts, mitochondrial respiration, and production of reactive oxygen species (ROS). Right ventricular functions were impaired while pulmonary right ventricular systolic pressure (RVSP) was amplified in hypoxia-exposed Nfat5(SMC)-/- versus Nfat5fl/fl mice. Scavenging of mitochondrial ROS normalized the raise in RVSP. Our findings suggest a critical role for NFAT5 as a suppressor of OXPHOS-associated gene expression, mitochondrial respiration, and ROS production in pulmonary artery SMCs that is vital to limit ROS-dependent arterial resistance in a hypoxic environment.

    DOI: 10.3390/cells10123293

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  8. Ferroptosis-dependent extracellular vesicles from macrophage contribute to asbestos-induced mesothelial carcinogenesis through loading ferritin Reviewed International journal

    Fumiya Ito, Katsuhiro Kato, Izumi Yanatori, Toyoaki Murohara, Shinya Toyokuni

    Redox Biology   Vol. 47   page: 102174 - 102174   2021.11

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    Asbestos-associated diseases remain a social burden worldwide. Our previous studies identified asbestos-induced iron-rich milieu for mesothelial cells with ceaseless macrophage ferroptosis. However, molecular mechanisms how this mutagenic milieu influences mesothelial cells have not been elucidated yet. Here, we propose a novel mechanism that extracellular vesicles (EVs) mediate asbestos-associated mutagenic factors to mesothelial cells. In a mice model of intraperitoneal crocidolite injection, mutagenic milieu highly expressed CD63, an exosomal marker. We then used a GFP-CD63 labeled THP-1 macrophage model exposed to crocidolite/iron, which generated EVs under ferroptotic process. We observed that MeT-5A mesothelial cells can receive and internalize these EVs. Furthermore, we comprehensively analyzed the ferroptosis-dependent EVs (FedEVs) for transported proteins and identified ferritin heavy/light chains as major components. Therefore, we inferred that FedEVs transport iron from ferroptotic macrophages to mesothelial cells. RNA sequencing revealed that the mesothelial cells receiving higher amounts of the FedEVs were mitotic, especially at the S and G2/M phases, by the use of Fucci mesothelial cells. Nuclear 8-hydroxy-2'-deoxyguanosine and γ-H2AX were significantly increased in the recipient mesothelial cells after exposure to FedEVs. Collectively, we here demonstrate a novel mechanism that FedEVs act as a key mutagenic mediator by transporting iron, which contribute to asbestos-induced mesothelial carcinogenesis.

    DOI: 10.1016/j.redox.2021.102174

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  9. Adverse Effect of Circadian Rhythm Disorder on Reparative Angiogenesis in Hind Limb Ischemia. Reviewed International coauthorship International journal

    Kazuhito Tsuzuki, Yuuki Shimizu, Junya Suzuki, Zhongyue Pu, Shukuro Yamaguchi, Yusuke Fujikawa, Katsuhiro Kato, Koji Ohashi, Mikito Takefuji, Yasuko K Bando, Noriyuki Ouchi, John W Calvert, Rei Shibata, Toyoaki Murohara

    Journal of the American Heart Association   Vol. 10 ( 16 ) page: e020896   2021.8

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    Background Circadian rhythm disorders, often seen in modern lifestyles, are a major social health concern. The aim of this study was to examine whether circadian rhythm disorders would influence angiogenesis and blood perfusion recovery in a mouse model of hind limb ischemia. Methods and Results A jet-lag model was established in C57BL/6J mice using a light-controlled isolation box. Control mice were kept at a light/dark 12:12 (12-hour light and 12-hour dark) condition. Concentrations of plasma vascular endothelial growth factor and circulating endothelial progenitor cells in control mice formed a circadian rhythm, which was diminished in the jet-lag model (P<0.05). The jet-lag condition deteriorated tissue capillary formation (P<0.001) and tissue blood perfusion recovery (P<0.01) in hind limb ischemia, which was associated with downregulation of vascular endothelial growth factor expression in local ischemic tissue and in the plasma. Although the expression of clock genes (ie, Clock, Bmal1, and Cry) in local tissues was upregulated after ischemic injury, the expression levels of cryptochrome (Cry) 1 and Cry2 were inhibited by the jet-lag condition. Next, Cry1 and Cry2 double-knockout mice were examined for blood perfusion recoveries and a reparative angiogenesis. Cry1 and Cry2 double-knockout mice revealed suppressed capillary density (P<0.001) and suppressed tissue blood perfusion recovery (P<0.05) in the hind limb ischemia model. Moreover, knockdown of CRY1/2 in human umbilical vein endothelial cells was accompanied by increased expression of WEE1 and decreased expression of HOXC5. This was associated with decreased proliferative capacity, migration ability, and tube formation ability of human umbilical vein endothelial cells, respectively, leading to impairment of angiogenesis. Conclusions Our data suggest that circadian rhythm disorder deteriorates reparative ischemia-induced angiogenesis and that maintenance of circadian rhythm plays an important role in angiogenesis.

    DOI: 10.1161/JAHA.121.020896

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  10. Treatment with adipose-derived regenerative cells enhances ischemia-induced angiogenesis via exosomal microRNA delivery in mice. Reviewed

    Tomohiro Kato, Katsuhiro Kato, Yuuki Shimizu, Mikito Takefuji, Toyoaki Murohara

    Nagoya journal of medical science   Vol. 83 ( 3 ) page: 465 - 476   2021.8

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    Adipose-derived regenerative cells (ADRCs), mesenchymal stem/progenitor cells from subcutaneous adipose tissue, have been shown to stimulate angiogenesis in hind limb ischemia, an effect attributed to paracrine action on endothelial cells (ECs) in mice. Despite promising therapeutic effects, the relevant molecules promoting neovascularization in this setting have not been fully elucidated. Extracellular vesicles, crucial mediators of intercellular communication, are recognized as a new therapeutic modality for regenerative medicine. Here, we found that GW4869, an exosome biogenesis inhibitor targeting neutral sphingomyelinase, impaired ADRCs-mediated angiogenesis and improvement of blood perfusion in a murine hind limb ischemia model. In addition, while the supernatant of ADRCs induced murine EC migration, this effect was attenuated by pre-treatment with GW4869. RNA analysis revealed that treatment of ADRCs with GW4869 reduced the expression of microRNA-21 (miR-21), miR-27b, miR-322, and let-7i in ADRCs-derived exosomes. Furthermore, the exosomes derived from GW4869-treated ADRCs induced the expression of the miR-21 targets Smad7 and Pten, and the miR-322 target Cul2, in ECs. These findings suggest that several miRNAs in ADRCs-derived exosomes contribute to angiogenesis and improvement of blood perfusion in a murine hind limb ischemia model.

    DOI: 10.18999/nagjms.83.3.465

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  11. Meflin defines mesenchymal stem cells and/or their early progenitors with multilineage differentiation capacity. Reviewed International journal

    Akitoshi Hara, Katsuhiro Kato, Toshikazu Ishihara, Hiroki Kobayashi, Naoya Asai, Shinji Mii, Yukihiro Shiraki, Yuki Miyai, Ryota Ando, Yasuyuki Mizutani, Tadashi Iida, Mikito Takefuji, Toyoaki Murohara, Masahide Takahashi, Atsushi Enomoto

    Genes to cells : devoted to molecular & cellular mechanisms   Vol. 26 ( 7 ) page: 495 - 512   2021.7

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    Mesenchymal stem cells (MSCs) are the likely precursors of multiple lines of mesenchymal cells. The existence of bona fide MSCs with self-renewal capacity and differentiation potential into all mesenchymal lineages, however, has been unclear because of the lack of MSC-specific marker(s) that are not expressed by the terminally differentiated progeny. Meflin, a glycosylphosphatidylinositol-anchored protein, is an MSC marker candidate that is specifically expressed in rare stromal cells in all tissues. Our previous report showed that Meflin expression becomes down-regulated in bone marrow-derived MSCs cultured on plastic, making it difficult to examine the self-renewal and differentiation of Meflin-positive cells at the single-cell level. Here, we traced the lineage of Meflin-positive cells in postnatal and adult mice, showing that those cells differentiated into white and brown adipocytes, osteocytes, chondrocytes and skeletal myocytes. Interestingly, cells derived from Meflin-positive cells formed clusters of differentiated cells, implying the in situ proliferation of Meflin-positive cells or their lineage-committed progenitors. These results, taken together with previous findings that Meflin expression in cultured MSCs was lost upon their multilineage differentiation, suggest that Meflin is a useful potential marker to localize MSCs and/or their immature progenitors in multiple tissues.

    DOI: 10.1111/gtc.12855

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  12. Omentin attenuates angiotensin II-induced abdominal aortic aneurysm formation in apolipoprotein E-knockout mice Reviewed

    Lixin Fang, Koji Ohashi, Naoya Otaka, Hayato Ogawa, Mizuho Hiramatsu-Ito, Hiroshi Kawanishi, Yasuko K Bando, Rei Shibata, Yuuki Shimizu, Katsuhiro Kato, Tomonobu Takikawa, Yuta Ozaki, Mikito Takefuji, Toyoaki Murohara, Noriyuki Ouchi

    Cardiovascular Research     2021.5

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    DOI: 10.1093/cvr/cvab179

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  13. Angiocrine FSTL1 (Follistatin-Like Protein 1) Insufficiency Leads to Atrial and Venous Wall Fibrosis via SMAD3 Activation. Reviewed International coauthorship International journal

    Haijuan Jiang, Luqing Zhang, Xuelian Liu, Wei Sun, Katsuhiro Kato, Chuankai Chen, Xiao Li, Taotao Li, Zhiliang Sun, Wencan Han, Fujing Zhang, Qi Xiao, Zhongzhou Yang, Junhao Hu, Zhihai Qin, Ralf H Adams, Xiang Gao, Yulong He

    Arteriosclerosis, thrombosis, and vascular biology   Vol. 40 ( 4 ) page: 958 - 972   2020.4

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    OBJECTIVE: Angiocrine factors, mediating the endothelial-mural cell interaction in vascular wall construction as well as maintenance, are incompletely characterized. This study aims to investigate the role of endothelial cell-derived FSTL1 (follistatin-like protein 1) in vascular homeostasis. Approach and Results: Using conditional knockout mouse models, we show that loss of FSTL1 in endothelial cells (Fstl1
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    ) led to an increase of pulmonary vascular resistance, resulting in the heart regurgitation especially with tricuspid valves. However, this abnormality was not detected in mutant mice with Fstl1 knockout in smooth muscle cells or hematopoietic cells. We further showed that there was excessive αSMA (α-smooth muscle actin) associated with atrial endocardia, heart valves, veins, and microvessels after the endothelial FSTL1 deletion. There was also an increase in collagen deposition, as demonstrated in livers of Fstl1
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    mutants. The SMAD3 (mothers against decapentaplegic homolog 3) phosphorylation (pSMAD3) was significantly enhanced, and pSMAD3 staining was colocalized with αSMA in vein walls, suggesting the activation of TGFβ (transforming growth factor β) signaling in vascular mural cells of Fstl1
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    mice. Consistently, treatment with a TGFβ pathway inhibitor reduced the abnormal association of αSMA with the atria and blood vessels in Fstl1
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    mutant mice. CONCLUSIONS: The findings imply that endothelial FSTL1 is critical for the homeostasis of vascular walls, and its insufficiency may favor cardiovascular fibrosis leading to heart failure.

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  14. YAP1 and TAZ negatively control bone angiogenesis by limiting hypoxia-inducible factor signaling in endothelial cells. Reviewed International coauthorship International journal

    Kishor K Sivaraj, Backialakshmi Dharmalingam, Vishal Mohanakrishnan, Hyun-Woo Jeong, Katsuhiro Kato, Silke Schröder, Susanne Adams, Gou Young Koh, Ralf H Adams

    eLife   Vol. 9   2020.1

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    Blood vessels are integrated into different organ environments with distinct properties and physiology (Augustin and Koh, 2017). A striking example of organ-specific specialization is the bone vasculature where certain molecular signals yield the opposite effect as in other tissues (Glomski et al., 2011; Kusumbe et al., 2014; Ramasamy et al., 2014). Here, we show that the transcriptional coregulators Yap1 and Taz, components of the Hippo pathway, suppress vascular growth in the hypoxic microenvironment of bone, in contrast to their pro-angiogenic role in other organs. Likewise, the kinase Lats2, which limits Yap1/Taz activity, is essential for bone angiogenesis but dispensable in organs with lower levels of hypoxia. With mouse genetics, RNA sequencing, biochemistry, and cell culture experiments, we show that Yap1/Taz constrain hypoxia-inducible factor 1α (HIF1α) target gene expression in vivo and in vitro. We propose that crosstalk between Yap1/Taz and HIF1α controls angiogenesis depending on the level of tissue hypoxia, resulting in organ-specific biological responses.

    DOI: 10.7554/eLife.50770

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  15. Indoxyl Sulfate-induced Vascular Calcification is mediated through Altered Notch Signaling Pathway in Vascular Smooth Muscle Cells. Reviewed International journal

    Kazutoshi Yamaguchi, Maimaiti Yisireyili, Sumie Goto, Katsuhiro Kato, Xian Wu Cheng, Takayuki Nakayama, Tadashi Matsushita, Toshimitsu Niwa, Toyoaki Murohara, Kyosuke Takeshita

    International journal of medical sciences   Vol. 17 ( 17 ) page: 2703 - 2717   2020

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    Introduction: The aim of this study was to determine the role of Notch in indoxyl sulfate (IS)-induced vascular calcification (VC). Materials and methods: VC and expression of Notch-related and osteogenic molecules were examined in Dahl salt-sensitive (DS), DS hypertensive (DH), and DH IS-treated rats (DH+IS). The effects of IS on expression of Notch receptors, apoptotic activity, and calcification were examined in cultured aortic smooth muscle cells (SMCs). Results: Medial calcification was noted only in aortas and coronary arteries of DH+IS rats. Notch1, Notch3, and Hes-1 were expressed in aortic SMCs of all rats, but only weakly in the central areas of the media and around the calcified lesions in DH+IS rats. RT-PCR and western blotting of DH+IS rat aortas showed downregulation of Notch ligands, Notch1 and Notch3, downstream transcriptional factors, and SM22, and conversely, overexpression of osteogenic markers. Expression of Notch1 and Notch3 in aortic SMCs was highest in incubation under 500 μM IS for 24hrs, and then decreased time- and dose-dependently. Coupled with this decrease, IS increased caspase 3/7 activity and TUNEL-positive aortic SMCs. In addition, pharmacological Notch signal inhibition with DAPT induced apoptosis in aortic SMCs. ZVAD, a caspase inhibitor abrogated IS-induced and DAPT-induced in vitro vascular calcification. Knockdown of Notch1 and Notch3 cooperatively increased expression of osteogenic transcriptional factors and decreased expression of SM22. Conclusion: Our results suggested that IS-induced VC is mediated through suppression of Notch activity in aortic SMCs, induction of osteogenic differentiation and apoptosis.

    DOI: 10.7150/ijms.43184

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  16. Endothelial EphB4 maintains vascular integrity and transport function in adult heart. Reviewed International coauthorship International journal

    Guillermo Luxán, Jonas Stewen, Noelia Díaz, Katsuhiro Kato, Sathish K Maney, Anusha Aravamudhan, Frank Berkenfeld, Nina Nagelmann, Hannes Ca Drexler, Dagmar Zeuschner, Cornelius Faber, Hermann Schillers, Sven Hermann, John Wiseman, Juan M Vaquerizas, Mara E Pitulescu, Ralf H Adams

    eLife   Vol. 8   2019.11

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    The homeostasis of heart and other organs relies on the appropriate provision of nutrients and functional specialization of the local vasculature. Here, we have used mouse genetics, imaging and cell biology approaches to investigate how homeostasis in the adult heart is controlled by endothelial EphB4 and its ligand ephrin-B2, which are known regulators of vascular morphogenesis and arteriovenous differentiation during development. We show that inducible and endothelial cell-specific inactivation of Ephb4 in adult mice is compatible with survival, but leads to rupturing of cardiac capillaries, cardiomyocyte hypertrophy, and pathological cardiac remodeling. In contrast, EphB4 is not required for integrity and homeostasis of capillaries in skeletal muscle. Our analysis of mutant mice and cultured endothelial cells shows that EphB4 controls the function of caveolae, cell-cell adhesion under mechanical stress and lipid transport. We propose that EphB4 maintains critical functional properties of the adult cardiac vasculature and thereby prevents dilated cardiomyopathy-like defects.

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  17. Protein Kinase N Promotes Stress-Induced Cardiac Dysfunction Through Phosphorylation of Myocardin-Related Transcription Factor A and Disruption of Its Interaction With Actin. Reviewed International coauthorship International journal

    Sakaguchi T, Takefuji M, Wettschureck N, Hamaguchi T, Amano M, Kato K, Tsuda T, Eguchi S, Ishihama S, Mori Y, Yura Y, Yoshida T, Unno K, Okumura T, Ishii H, Shimizu Y, Bando YK, Ohashi K, Ouchi N, Enomoto A, Offermanns S, Kaibuchi K, Murohara T

    Circulation   Vol. 140 ( 21 ) page: 1737 - 1752   2019.11

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    Background: Heart failure is a complex syndrome that results from structural or functional impairment of ventricular filling or blood ejection. Protein phosphorylation is a major and essential intracellular mechanism that mediates various cellular processes in cardiomyocytes in response to extracellular and intracellular signals. The RHOA-associated protein kinase (ROCK/Rho-kinase), an effector regulated by the small GTPase RHOA, causes pathological phosphorylation of proteins, resulting in cardiovascular diseases. RHOA also activates protein kinase N (PKN); however, the role of PKN in cardiovascular diseases remains unclear. Methods: To explore the role of PKNs in heart failure, we generated tamoxifen-inducible, cardiomyocyte-specific PKN1- and PKN2-knockout mice by intercrossing the alpha MHC-CreERT2 line with Pkn1(flox/flox) and Pkn2(flox/flox) mice and applied a mouse model of transverse aortic constriction- and angiotensin II-induced heart failure. To identify a novel substrate of PKNs, we incubated GST-tagged myocardin-related transcription factor A (MRTFA) with recombinant GST-PKN-catalytic domain or GST-ROCK-catalytic domain in the presence of radiolabeled ATP and detected radioactive GST-MRTFA as phosphorylated MRTFA. Results: We demonstrated that RHOA activates 2 members of the PKN family of proteins, PKN1 and PKN2, in cardiomyocytes of mice with cardiac dysfunction. Cardiomyocyte-specific deletion of the genes encoding Pkn1 and Pkn2 (cmc-PKN1/2 DKO) did not affect basal heart function but protected mice from pressure overload- and angiotensin II-induced cardiac dysfunction. Furthermore, we identified MRTFA as a novel substrate of PKN1 and PKN2 and found that MRTFA phosphorylation by PKN was considerably more effective than that by ROCK in vitro. We confirmed that endogenous MRTFA phosphorylation in the heart was induced by pressure overload- and angiotensin II-induced cardiac dysfunction in wild-type mice, whereas cmc-PKN1/2 DKO mice suppressed transverse aortic constriction- and angiotensin II-induced phosphorylation of MRTFA. Although RHOA-mediated actin polymerization accelerated MRTFA-induced gene transcription, PKN1 and PKN2 inhibited the interaction of MRTFA with globular actin by phosphorylating MRTFA, causing increased serum response factor-mediated expression of cardiac hypertrophy- and fibrosis-associated genes. Conclusions: Our results indicate that PKN1 and PKN2 activation causes cardiac dysfunction and is involved in the transition to heart failure, thus providing unique targets for therapeutic intervention for heart failure.

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  18. Roles of the Mesenchymal Stromal/Stem Cell Marker Meflin in Cardiac Tissue Repair and the Development of Diastolic Dysfunction. Reviewed International journal

    Akitoshi Hara, Hiroki Kobayashi, Naoya Asai, Shigeyoshi Saito, Takahiro Higuchi, Katsuhiro Kato, Takahiro Okumura, Yasuko K Bando, Mikito Takefuji, Yasuyuki Mizutani, Yuki Miyai, Shoji Saito, Shoichi Maruyama, Keiko Maeda, Noriyuki Ouchi, Arata Nagasaka, Takaki Miyata, Shinji Mii, Noriyuki Kioka, Daniel L Worthley, Toyoaki Murohara, Masahide Takahashi, Atsushi Enomoto

    Circulation research   Vol. 125 ( 4 ) page: 414 - 430   2019.8

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    RATIONALE: Myofibroblasts have roles in tissue repair following damage associated with ischemia, aging, and inflammation and also promote fibrosis and tissue stiffening, causing organ dysfunction. One source of myofibroblasts is mesenchymal stromal/stem cells that exist as resident fibroblasts in multiple tissues. We previously identified meflin (mesenchymal stromal cell- and fibroblast-expressing Linx paralogue), a glycosylphosphatidylinositol-anchored membrane protein, as a specific marker of mesenchymal stromal/stem cells and a regulator of their undifferentiated state. The roles of meflin in the development of heart disease, however, have not been investigated. OBJECTIVE: We examined the expression of meflin in the heart and its involvement in cardiac repair after ischemia, fibrosis, and the development of heart failure. METHODS AND RESULTS: We found that meflin has an inhibitory role in myofibroblast differentiation of cultured mesenchymal stromal/stem cells. Meflin expression was downregulated by stimulation with TGF (transforming growth factor)-β, substrate stiffness, hypoxia, and aging. Histological analysis revealed that meflin-positive fibroblastic cells and their lineage cells proliferated in the hearts after acute myocardial infarction and pressure-overload heart failure mouse models. Analysis of meflin knockout mice revealed that meflin is essential for the increase in the number of cells that highly express type I collagen in the heart walls after myocardial infarction induction. When subjected to pressure overload by transverse aortic constriction, meflin knockout mice developed marked cardiac interstitial fibrosis with defective compensation mechanisms. Analysis with atomic force microscopy and hemodynamic catheterization revealed that meflin knockout mice developed stiff failing hearts with diastolic dysfunction. Mechanistically, we found that meflin interacts with bone morphogenetic protein 7, an antifibrotic cytokine that counteracts the action of TGF-β and augments its intracellular signaling. CONCLUSIONS: These data suggested that meflin is involved in cardiac tissue repair after injury and has an inhibitory role in myofibroblast differentiation of cardiac fibroblastic cells and the development of cardiac fibrosis.

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  19. Focused Proteomics Revealed a Novel Rho-kinase Signaling Pathway in the Heart Reviewed

    Yura, Y. Amano, M. Takefuji, M. Bando, T. Suzuki, K. Kato, K. Hamaguchi, T. Hasanuzzaman Shohag, M. Takano, T. Funahashi, Y. Nakamuta, S. Kuroda, K. Nishioka, T. Murohara, T. Kaibuchi, K

    Cell Struct Funct   Vol. 41 ( 2 ) page: 105-120 - 120   2016.8

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    Protein phosphorylation plays an important role in the physiological regulation of cardiac function. Myocardial contraction and pathogenesis of cardiac diseases have been reported to be associated with adaptive or maladaptive protein phosphorylation; however, phosphorylation signaling in the heart is not fully elucidated. We recently developed a novel kinase-interacting substrate screening (KISS) method for exhaustive screening of protein kinase substrates, using mass spectrometry and affinity chromatography. First, we examined protein phosphorylation by extracellular signal-regulated kinase (ERK) and protein kinase A (PKA), which has been relatively well studied in cardiomyocytes. The KISS method showed that ERK and PKA mediated the phosphorylation of known cardiac-substrates of each kinase such as Rps6ka1 and cTnI, respectively. Using this method, we found about 330 proteins as Rho-kinase-mediated substrates, whose substrate in cardiomyocytes is unknown. Among them, CARP/Ankrd1, a muscle ankyrin repeat protein, was confirmed as a novel Rho-kinase-mediated substrate. We also found that non-phosphorylatable form of CARP repressed cardiac hypertrophy-related gene Myosin light chain-2v (MLC-2v) promoter activity, and decreased cell size of heart derived H9c2 myoblasts more efficiently than wild type-CARP. Thus, focused proteomics enable us to reveal a novel signaling pathway in the heart.

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  20. C3G/Rapgef1 Is Required in Multipolar Neurons for the Transition to a Bipolar Morphology during Cortical Development Reviewed International coauthorship International journal

    Bhavin Shah, Daniela Lutter, Magdalena L. Bochenek, Katsuhiro Kato, Yaroslav Tsytsyura, Natalia Glyvuk, Akira Sakakibara, Juergen Klingauf, Ralf H. Adams, Andreas W. Pueschel

    PLOS ONE   Vol. 11 ( 4 ) page: e0154174   2016.4

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    The establishment of a polarized morphology is essential for the development and function of neurons. During the development of the mammalian neocortex, neurons arise in the ventricular zone (VZ) from radial glia cells (RGCs) and leave the VZ to generate the cortical plate (CP). During their migration, newborn neurons first assume a multipolar morphology in the subventricular zone (SVZ) and lower intermediate zone (IZ). Subsequently, they undergo a multi-to-bipolar (MTB) transition to become bipolar in the upper IZ by developing a leading process and a trailing axon. The small GTPases Rap1A and Rap1B act as master regulators of neural cell polarity in the developing mouse neocortex. They are required for maintaining the polarity of RGCs and directing the MTB transition of multipolar neurons. Here we show that the Rap1 guanine nucleotide exchange factor (GEF) C3G (encoded by the Rapgef1 gene) is a crucial regulator of the MTB transition in vivo by conditionally inactivating the Rapgef1 gene in the developing mouse cortex at different time points during neuronal development. Inactivation of C3G results in defects in neuronal migration, axon formation and cortical lamination. Live cell imaging shows that C3G is required in cortical neurons for both the specification of an axon and the initiation of radial migration by forming a leading process.

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  21. Regulation of Vascular Endothelial Growth Factor Receptor Function in Angiogenesis by Numb and Numb-Like Reviewed International journal

    Max van Lessen, Masanori Nakayama, Katsuhiro Kato, Jung Mo Kim, Kozo Kaibuchi, Ralf H. Adams

    ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY   Vol. 35 ( 8 ) page: 1815 - 1825   2015.8

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    Objective Vascular endothelial growth factor (VEGF) signaling is a major regulator of physiological and pathological angiogenesis. VEGF receptor activity is strongly controlled by endocytosis, which can terminate or enhance signal transduction in the angiogenic endothelium, but the exact molecular regulation of these processes remains incompletely understood. We have therefore examined the function of Numb family clathrin-associated sorting proteins in angiogenesis.
    Approach and Results We show that Numb proteins are expressed by endothelial cells during retinal angiogenesis in mice. Inducible inactivation of the Numb/Numbl genes in the postnatal endothelium led to impaired vessel growth, reduced endothelial proliferation and sprouting, and decreased VEGF receptor activation. Biochemistry and cell biology experiments established that Numb can interact with VEGFR2 and VEGFR3 and controls VEGF receptor activation in response to ligand stimulation. Experiments in cultured endothelial cells showed that Numb proteins counteract VEGF receptor degradation and promote VEGFR2 recycling back to the plasma membrane.
    Conclusions Numb proteins control VEGF receptor endocytosis, signaling, and recycling in endothelial cells, which promotes the angiogenic growth of blood vessels.

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  22. Kinase-interacting substrate screening is a novel method to identify kinase substrates Reviewed International journal

    Amano, M, Hamaguchi, T, Shohag, M. H, Kozawa, K, Kato, K, Zhang, X, Yura, Y, Matsuura, Y, Kataoka, C, Nishioka, T, Kaibuchi, K

    J Cell Biol   Vol. 209 ( 6 ) page: 895-912 - 912   2015.6

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    Protein kinases play pivotal roles in numerous cellular functions; however, the specific substrates of each protein kinase have not been fully elucidated. We have developed a novel method called kinase-interacting substrate screening (KISS). Using this method, 356 phosphorylation sites of 140 proteins were identified as candidate substrates for Rho-associated kinase (Rho-kinase/ROCK2), including known substrates. The KISS method was also applied to additional kinases, including PKA, MAPK1, CDK5, CaMK1, PAK7, PKN, LYN, and FYN, and a lot of candidate substrates and their phosphorylation sites were determined, most of which have not been reported previously. Among the candidate substrates for Rho-kinase, several functional clusters were identified, including the polarity-associated proteins, such as Scrib. We found that Scrib plays a crucial role in the regulation of subcellular contractility by assembling into a ternary complex with Rho-kinase and Shroom2 in a phosphorylation-dependent manner. We propose that the KISS method is a comprehensive and useful substrate screen for various kinases.

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  23. Integrin beta 1 controls VE-cadherin localization and blood vessel stability Reviewed International coauthorship International journal

    Hiroyuki Yamamoto, Manuel Ehling, Katsuhiro Kato, Kenichi Kanai, Max van Lessen, Maike Frye, Dagmar Zeuschner, Masanori Nakayama, Dietmar Vestweber, Ralf H. Adams

    NATURE COMMUNICATIONS   Vol. 6   page: 6429 - 6429   2015.3

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    Angiogenic blood vessel growth requires several distinct but integrated cellular activities. Endothelial cell sprouting and proliferation lead to the expansion of the vasculature and give rise to a highly branched, immature plexus, which is subsequently reorganized into a mature and stable network. Although it is known that integrin-mediated cell-matrix interactions are indispensable for embryonic angiogenesis, little is known about the function of integrins in different steps of vascular morphogenesis. Here, by investigating the integrin beta 1-subunit with inducible and endothelial-specific gene targeting in the postnatal mouse retina, we show that beta 1 integrin promotes endothelial sprouting but is a negative regulator of proliferation. In maturing vessels, integrin beta 1 is indispensable for proper localization of VE-cadherin and thereby cell-cell junction integrity. The sum of our findings establishes that integrin beta 1 has critical functions in the growing and maturing vasculature, and is required for the formation of stable, non-leaky blood vessels.

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  24. ERK2-Mediated Phosphorylation of Par3 Regulates Neuronal Polarization Reviewed International journal

    Yasuhiro Funahashi, Takashi Namba, Shin Fujisue, Norimichi Itoh, Shinichi Nakamuta, Katsuhiro Kato, Akiko Shimada, Chundi Xu, Wei Shan, Tomoki Nishioka, Kozo Kaibuchi

    JOURNAL OF NEUROSCIENCE   Vol. 33 ( 33 ) page: 13270 - 13285   2013.8

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    Axon formation is one of the most important events in neuronal polarization and is regulated by signaling molecules involved in cytoskeletal rearrangement and protein transport. We previously found that Partition-defective 3 (Par3) is associated with KIF3A (kinesin-2) and is transported into the nascent axon in a KIF3A-dependent fashion. Par3 interacts with the Rac-specific guanine nucleotide-exchange factors (GEFs) Tiam1/2, which activate Rac1, and participates in axon formation in cultured hippocampal neurons. However, the regulatory mechanism of the Par3-KIF3A interaction is poorly understood, and the role of Par3 in neuronal polarization in vivo remains elusive. Here, we found that extracellular signal-regulated kinase 2 (ERK2) directly interacts with Par3, that ERK2 phosphorylates Par3 at Ser-1116, and that the phosphorylated Par3 accumulates at the axonal tips in a manner dependent upon ERK2 activity. The phosphorylation of Par3 by ERK2 inhibited the interaction of Par3 with KIF3A but not with the other Par3 partners, including Par6 and aPKC. The phosphomimic mutant of Par3 (Par3-S1116D) showed less binding activity with the KIF3s and slower transport in the axons. The knockdown of Par3 by RNA interference impaired neuronal polarization, which was rescued with RNAi-resistant Par3, but not with the phosphomimic Par3 mutant, in cultured rat hippocampal neurons and mouse cortical projection neurons in vivo. These results suggest that ERK2 phosphorylates Par3 and inhibits its binding with KIF3A, thereby controlling Par3 transport and neuronal polarity.

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  25. Treatment of sirolimus-eluting stent restenosis: Additional stent, balloon angioplasty, and coronary artery bypass graft Reviewed International journal

    Kiyotake Ishikawa, Yutaka Aoyama, Katsuhiro Kato, Akihito Tanaka, Mizuho Hiramatsu, Masayoshi Ajioka, Haruo Kamiya, Toshikazu Tanaka, Haruo Hirayama

    Journal of Cardiac Surgery   Vol. 28 ( 2 ) page: 97 - 101   2013.3

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    Objective: Sirolimus-eluting stent (SES) has shown a significant efficacy in reducing restenosis after percutaneous coronary interventions. However, an increase in total number of SES use along with targeting more complex lesions generated a large number of SES restenosis. This study aimed to investigate the clinical and angiographic outcomes of different revascularization strategies for SES restenosis. Methods and Results: A total of 176 lesions in 149 patients were included in the study. Fifteen patients underwent coronary artery bypass graft surgery (CABG group) and the remaining patients were treated with percutaneous coronary intervention (PCI). Stent reimplantation was performed in 88 patients (Stent group), whereas 46 patients received balloon therapy (Balloon group). Among 176 lesions, major cardiac adverse event (MACE) occurred in 41 lesions (23.3%) during a median follow-up of 310 days (interquartile range: 146-517 days). The Kaplan-Meier method with a log-rank test revealed no significant difference in MACE rates between the three groups (6%, 25%, 26%, p = 0.13
    CABG group, Stent group, Balloon group, respectively). However, when the Balloon group and Stent group were combined together as a PCI group, PCI group had a significantly higher rate of MACE compared with the CABG group (p = 0.04). In addition, angiographic restenosis was significantly less prevalent in the CABG group when compared with the other two groups (8%, 57%, 46%, p = 0.006
    CABG group, Stent group, Balloon group, respectively). Conclusions: CABG surgery for patients with SES restenosis is associated with the better clinical outcomes as well as better angiographic outcomes when compared with that of PCI. © 2013 Wiley Periodicals, Inc.

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  26. [Small GTPases and their effectors]. Reviewed

    Kato K, Amano M, Kaibuchi K

    Nihon rinsho. Japanese journal of clinical medicine   Vol. 70 Suppl 8   page: 67 - 70   2012.11

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  27. Distinct distribution and localization of Rho-kinase in mouse epithelial, muscle and neural tissues Reviewed

    Iizuka, M, Kimura, K, Wang, S, Kato, K, Amano, M, Kaibuchi, K, Mizoguchi, A

    Cell Struct Funct   Vol. 37 ( 2 ) page: 155-175   2012.9

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    The small GTP-binding protein Rho plays a crucial role in a wide variety of cellular functions through various effector proteins. Rho-kinase is a key effector protein of Rho, which is composed of two isoforms, ROCK1 and ROCK2. To clarify the site of action of ROCK1 and ROCK2, we performed immunofluorescence and immunoelectron microscopic analyses using isoform-specific antibodies in mouse tissues. In the large and small intestines, ROCK1 immunoreactivity was predominantly identified in epithelial cells, and ROCK2 immunoreactivity was negligible. In these epithelial cells, ROCK1 immunoreactivity was distributed on plasma membranes, while ROCK1 immunogold signals were localized at cell-cell contacts and cell adhesion sites, especially at the adherens junctions at the ultrastructural level. In the bladder epithelium, however, ROCK1 and ROCK2 signals were identified at intermediate filaments, and ROCK2 signals were also observed in nuclei. In the three types of muscular cells - smooth, cardiac, and skeletal muscle cells - ROCK1 and ROCK2 also showed differential distribution. ROCK1 signals were localized at actin filaments, plasma membranes, and vesicles near plasma membranes in smooth

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  28. The inositol 5-phosphatase SHIP2 is an effector of RhoA and is involved in cell polarity and migration Reviewed International journal

    Katsuhiro Kato, Tsubasa Yazawa, Kentaro Taki, Kazutaka Mori, Shujie Wang, Tomoki Nishioka, Tomonari Hamaguchi, Toshiki Itoh, Tadaomi Takenawa, Chikako Kataoka, Yoshiharu Matsuura, Mutsuki Amano, Toyoaki Murohara, Kozo Kaibuchi

    MOLECULAR BIOLOGY OF THE CELL   Vol. 23 ( 13 ) page: 2593 - 2604   2012.7

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    Cell migration is essential for various physiological and pathological processes. Polarization in motile cells requires the coordination of several key signaling molecules, including RhoA small GTPases and phosphoinositides. Although RhoA participates in a front-rear polarization in migrating cells, little is known about the functional interaction between RhoA and lipid turnover. We find here that src-homology 2-containing inositol-5-phosphatase 2 (SHIP2) interacts with RhoA in a GTP-dependent manner. The association between SHIP2 and RhoA is observed in spreading and migrating U251 glioma cells. The depletion of SHIP2 attenuates cell polarization and migration, which is rescued by wild-type SHIP2 but not by a mutant defective in RhoA binding. In addition, the depletion of SHIP2 impairs the proper localization of phosphatidylinositol 3,4,5-trisphosphate, which is not restored by a mutant defective in RhoA binding. These results suggest that RhoA associates with SHIP2 to regulate cell polarization and migration.

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  29. Involvement of Girdin in the Determination of Cell Polarity during Cell Migration Reviewed International journal

    Kei Ohara, Atsushi Enomoto, Takuya Kato, Takahiko Hashimoto, Mayu Isotani-Sakakibara, Naoya Asai, Maki Ishida-Takagishi, Liang Weng, Masanori Nakayama, Takashi Watanabe, Katsuhiro Kato, Kozo Kaibuchi, Yoshiki Murakumo, Yoshiki Hirooka, Hidemi Goto, Masahide Takahashi

    PLOS ONE   Vol. 7 ( 5 ) page: e36681   2012.5

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    Cell migration is a critical cellular process that determines embryonic development and the progression of human diseases. Therefore, cell- or context-specific mechanisms by which multiple promigratory proteins differentially regulate cell migration must be analyzed in detail. Girdin (girders of actin filaments) (also termed GIV,G alpha-interacting vesicle associated protein) is an actin-binding protein that regulates migration of various cells such as endothelial cells, smooth muscle cells, neuroblasts, and cancer cells. Here we show that Girdin regulates the establishment of cell polarity, the deregulation of which may result in the disruption of directional cell migration. We found that Girdin interacts with Par-3, a scaffolding protein that is a component of the Par protein complex that has an established role in determining cell polarity. RNA interference-mediated depletion of Girdin leads to impaired polarization of fibroblasts and mammary epithelial cells in a way similar to that observed in Par-3-depleted cells. Accordingly, the expression of Par- 3 mutants unable to interact with Girdin abrogates cell polarization in fibroblasts. Further biochemical analysis suggests that Girdin is present in the Par protein complex that includes Par-3, Par-6, and atypical protein kinase C. Considering previous reports showing the role of Girdin in the directional migration of neuroblasts, network formation of endothelial cells, and cancer invasion, these data may provide a specific mechanism by which Girdin regulates cell movement in biological contexts that require directional cell movement.

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  30. Distinct distribution and localization of Rho-kinase in mouse epithelial, muscle and neural tissues. Reviewed

    Iizuka M, Kimura K, Wang S, Kato K, Amano M, Kaibuchi K, Mizoguchi A

    Cell structure and function   Vol. 37 ( 2 ) page: 155 - 175   2012

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    The small GTP-binding protein Rho plays a crucial role in a wide variety of cellular functions through various effector proteins. Rho-kinase is a key effector protein of Rho, which is composed of two isoforms, ROCK1 and ROCK2. To clarify the site of action of ROCK1 and ROCK2, we performed immunofluorescence and immunoelectron microscopic analyses using isoform-specific antibodies in mouse tissues. In the large and small intestines, ROCK1 immunoreactivity was predominantly identified in epithelial cells, and ROCK2 immunoreactivity was negligible. In these epithelial cells, ROCK1 immunoreactivity was distributed on plasma membranes, while ROCK1 immunogold signals were localized at cell-cell contacts and cell adhesion sites, especially at the adherens junctions at the ultrastructural level. In the bladder epithelium, however, ROCK1 and ROCK2 signals were identified at intermediate filaments, and ROCK2 signals were also observed in nuclei. In the three types of muscular cells-smooth, cardiac, and skeletal muscle cells-ROCK1 and ROCK2 also showed differential distribution. ROCK1 signals were localized at actin filaments, plasma membranes, and vesicles near plasma membranes in smooth muscle cells; at the lysosomes in skeletal muscle cells; and were undetectable in cardiac muscle cells. ROCK2 signals were localized at actin filaments and centrosomes in smooth muscle cells, at intercalated discs in cardiac muscle cells, and at Z-discs and sarcoplasmic reticulum in skeletal muscle cells. In the brain, ROCK1 immunoreactivity was distributed in glia, whereas ROCK2 immunoreactivity was observed in neurons. These results indicate that the two isoforms of Rho-kinase distribute differentially to accomplish their specific functions.

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  31. The Actin-Binding Protein Girdin and Its Akt-Mediated Phosphorylation Regulate Neointima Formation After Vascular Injury Reviewed

    Hiroshi Miyake, Kengo Maeda, Naoya Asai, Rei Shibata, Hitoshi Ichimiya, Mayu Isotani-Sakakibara, Yumiko Yamamura, Katsuhiro Kato, Atsushi Enomoto, Masahide Takahashi, Toyoaki Murohara

    CIRCULATION RESEARCH   Vol. 108 ( 10 ) page: 1170 - U65   2011.5

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    Rationale: It is well established that the migration and proliferation of vascular smooth muscle cells (VSMCs) have major roles in the vascular remodeling process. Our previous study showed that the Akt substrate Girdin, which is expressed in VSMCs and endothelial cells, is essential for postnatal angiogenesis. However, the function of Girdin and its Akt-mediated phosphorylation in VSMCs and their in vivo roles in vascular remodeling remain to be elucidated.
    Objective: We investigated the function of Girdin and its Akt-mediated phosphorylation using cultured VSMCs and animal models of vascular remodeling.
    Methods and Results: The depletion of Girdin by RNA interference disrupted the rearrangement of the actin cytoskeleton in VSMCs, resulting in impaired cell migration. The depletion of Girdin also inhibited VSMC proliferation. Girdin expression was highly upregulated and its serine at position 1416 was phosphorylated in the neointima of carotid arteries after balloon injury in a rat model. The introduction of an adenovirus harboring short hairpin RNA against Girdin attenuated the proliferation of VSMCs and neointima formation without affecting reendothelialization. Furthermore, we found that neointima formation after femoral wire injury was significantly attenuated in Girdin S1416A knock-in mice, in which the Akt phosphorylation site of Girdin was mutated, thus indicating a major role for Girdin phosphorylation in vascular remodeling.
    Conclusions: These findings indicate that Girdin and its Akt-mediated phosphorylation have major roles in the migration and proliferation of VSMCs and vascular remodeling, making the Akt/Girdin signaling pathway a potential target for the development of new therapeutics for vascular diseases. (Circ Res. 2011;108:1170-1179.)

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  32. Mutation of ARHGAP9 in patients with coronary spastic angina Reviewed

    Mikito Takefuji, Hiroyuki Asano, Kazutaka Mori, Mutsuki Amano, Katsuhiro Kato, Takashi Watanabe, Yasuhiro Morita, Akira Katsumi, Toshiki Itoh, Tadaomi Takenawa, Akihiro Hirashiki, Hideo Izawa, Kozo Nagata, Haruo Hirayama, Fumimaro Takatsu, Tomoki Naoe, Mitsuhiro Yokota, Kozo Kaibuchi

    JOURNAL OF HUMAN GENETICS   Vol. 55 ( 1 ) page: 42 - 49   2010.1

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    Coronary artery spasm has an important function in the etiology of variant angina and other acute coronary syndromes. Abnormal activation of Rho-family GTPases has been observed in cardiovascular disorders, but the function of genetic variability in Rho-family GTPases remains to be evaluated in cardiovascular disorders. We examined the genetic variability of Rho-family GTPases and their regulators in coronary artery spasm. We performed a comprehensive candidate gene analysis of 67 single nucleotide polymorphisms with amino-acid substitution in Rho-family GTPases and their regulators in 103 unrelated Japanese patients with acetylcholine-induced coronary artery spasm and 102 control Japanese subjects without acetylcholine-induced coronary artery spasm. We noted an association of the single nucleotide polymorphism of ARHGAP9 (rs11544238, Ala370Ser) with coronary artery spasm (odds ratio=2.67). We found that ARHGAP9 inactivated Rac as RacGAP and that the mRNA level of ARHGAP9 was strongly detected in hematopoietic cells. ARHGAP9 negatively regulated cell migration. The Ala370Ser polymorphism counteracted ARHGAP9-reduced cell migration, spreading and adhesion. The Ala370Ser polymorphism in the ARHGAP9 gene is associated with coronary artery spasm. These data suggest that the polymorphism of ARHGAP9 has a critical function in the infiltration of hematopoietic cells into the endothelium and inflammation leading to endothelial dysfunction. Journal of Human Genetics (2010) 55, 42-49; doi: 10.1038/jhg.2009.120; published online 13 November 2009

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  33. A Proteomic Approach for Comprehensively Screening Substrates of Protein Kinases Such as Rho-Kinase Reviewed

    Mutsuki Amano, Yuta Tsumura, Kentaro Taki, Hidenori Harada, Kazutaka Mori, Tomoki Nishioka, Katsuhiro Kato, Takeshi Suzuki, Yosuke Nishioka, Akihiro Iwamatsu, Kozo Kaibuchi

    PLOS ONE   Vol. 5 ( 1 ) page: e8704   2010.1

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    Background: Protein kinases are major components of signal transduction pathways in multiple cellular processes. Kinases directly interact with and phosphorylate downstream substrates, thus modulating their functions. Despite the importance of identifying substrates in order to more fully understand the signaling network of respective kinases, efficient methods to search for substrates remain poorly explored.
    Methodology/Principal Findings: We combined mass spectrometry and affinity column chromatography of the catalytic domain of protein kinases to screen potential substrates. Using the active catalytic fragment of Rho-kinase/ROCK/ROK as the model bait, we obtained about 300 interacting proteins from the rat brain cytosol fraction, which included the proteins previously reported as Rho-kinase substrates. Several novel interacting proteins, including doublecortin, were phosphorylated by Rho-kinase both in vitro and in vivo.
    Conclusions/Significance: This method would enable identification of novel specific substrates for kinases such as Rho-kinase with high sensitivity.

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  34. Rho-kinase Contributes to Sustained RhoA Activation through Phosphorylation of p190A RhoGAP Reviewed

    Kazutaka Mori, Mutsuki Amano, Mikito Takefuji, Katsuhiro Kato, Yasuhiro Morita, Tomoki Nishioka, Yoshiharu Matsuura, Toyoaki Murohara, Kozo Kaibuchi

    JOURNAL OF BIOLOGICAL CHEMISTRY   Vol. 284 ( 8 ) page: 5067 - 5076   2009.2

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    RhoA is transiently activated by specific extracellular signals such as endothelin-1 (ET-1) in vascular smooth muscle cells. RhoGAP negatively regulates RhoA activity: thus, RhoA becomes the GDP-bound inactive form afterward. Sustained activation of RhoA is induced with high doses of the extracellular signals and is implicated in certain diseases such as vasospasms. However, it remains largely unknown how prolonged activation of RhoA is induced. Here we show that Rho-kinase, an effector of RhoA, phosphorylated p190A RhoGAP at Ser(1150) and attenuated p190A RhoGAP activity in COS7 cells. Binding of Rnd to p190A RhoGAP is thought to enhance its activation. Phosphorylation of p190A RhoGAP by Rho-kinase impaired Rnd binding. Stimulation of vascular smooth muscle cells with a high dose of ET-1 provoked sustained RhoA activation and p190A RhoGAP phosphorylation, both of which were prohibited by a Rho-kinase inhibitor. The phosphomimic mutation of p190A RhoGAP weakened Rnd binding and RhoGAP activities. Taken together, these results suggest that ET-1 induces Rho-kinase activation and subsequent phosphorylation of p190A RhoGAP, leading to prolonged RhoA activation.

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  35. High frequency oscillatory ventilation(HFOV)が有効であったARDSの1例 Reviewed

    加藤 勝洋, 長谷川 隆一, 勝田 知也, 谷口 博之, 近藤 康博, 木村 智樹, 西山 理, 加藤 景介, 野間 聖, 岩木 舞, 阪本 考司, 麻生 裕紀, 横山 俊樹

    日本呼吸器学会雑誌   Vol. 44 ( 10 ) page: 732 - 737   2006.10

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    症例は69歳男性。急性前立腺炎にて入院後、血痰及び両側上肺野に浸潤影が出現した。呼吸器内科転科時、PaO2 57.3Torr,BALではNeu 15.6%,Ly 33.6%,Eo 26.6%,Mφ 23.6%で定量培養陰性。急速に呼吸状態が悪化しARDSとなったため、非侵襲的・侵襲的人工呼吸管理、ステロイドパルス療法・好中球エラスターゼ阻害剤投与を行ったが改善せず、第8病日よりHFOVを開始した。HFOV管理後急速に酸素化の改善がみられ、第17病日には人工呼吸管理から離脱でき救命し得た。ARDSに対しHFOVが有効であった貴重な症例であると考え報告する。(著者抄録)

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  36. Role of numb in dendritic spine development with a Cdc42 GEF intersectin and EphB2 Reviewed

    T Nishimura, T Yamaguchi, A Tokunaga, A Hara, T Hamaguchi, K Kato, A Lwamatsu, H Okano, K Kaibuchi

    MOLECULAR BIOLOGY OF THE CELL   Vol. 17 ( 3 ) page: 1273 - 1285   2006.3

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    Numb has been implicated in cortical neurogenesis during nervous system development, as a result of its asymmetric partitioning and antagonizing Notch signaling. Recent studies have revealed that Numb functions in clathrin-dependent endocytosis by binding to the AP-2 complex. Numb is also expressed in postmitotic neurons and plays a role in axonal growth. However, the functions of Numb in later stages of neuronal development remain unknown. Here, we report that Numb specifically localizes to dendritic spines in cultured hippocampal neurons and is implicated in dendritic spine morphogenesis, partially through the direct interaction with intersectin, a Cdc42 guanine nucleotide exchange factor (GEF) Intersectin functions as a multidomain adaptor for proteins involved in endocytosis and cytoskeletal regulation. Numb enhanced the GEF activity of intersectin toward Cdc42 in vivo. Expression of Numb or intersectin caused the elongation of spine neck, whereas knockdown of Numb and Numb-like decreased the protrusion density and its length. Furthermore, Numb formed a complex with EphB2 receptor-type tyrosine kinase and NMDA-type glutamate receptors. Knockdown of Numb suppressed the ephrin-B1-induced spine development and maturation. These results highlight a role of Numb for dendritic spine development and synaptic functions with intersectin and EphB2.

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  37. PAR-6-PAR-3 mediates Cdc42-induced Rac activation through the Rac GEFs STEF/Tiam1 Reviewed

    T Nishimura, T Yamaguchi, K Kato, M Yoshizawa, Y Nabeshima, S Ohno, M Hoshino, K Kaibuchi

    NATURE CELL BIOLOGY   Vol. 7 ( 3 ) page: 270 - U77   2005.3

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    A polarity complex of PAR-3, PAR-6 and atypical protein kinase C ( aPKC) functions in various cell-polarization events, including neuron specification(1-4). The small GTPase Cdc42 binds to PAR-6 and regulates cell polarity. However, little is known about the downstream signals of the Cdc42 - PAR protein complex. Here, we found that PAR-3 directly interacted with STEF/Tiam1, which are Rac-specific guanine nucleotide-exchange factors, and that STEF formed a complex with PAR-3 - aPKC - PAR-6 - Cdc42-GTP. Cdc42 induces lamellipodia in a Rac-dependent manner in N1E-115 neuroblastoma cells. Disruption of Cdc42 PAR- 6 or PAR- 3 - STEF binding inhibited Cdc42-induced lamellipodia but not filopodia. The isolated STEF-binding PAR-3 fragment was sufficient to induce lamellipodia independently of Cdc42 and PAR-6. PAR-3 is required for Cdc42-induced Rac activation, but is not essential for lamellipodia formation itself. In cultured hippocampal neurons, STEF accumulated at the tip of the growing axon and colocalized with PAR-3. The spatio-temporal activation and signalling of Cdc42 - PAR- 6 - PAR-3 - STEF/Tiam1 - Rac seem to be involved in neurite growth and axon specification. We propose that the PAR- 6 - PAR- 3 complex mediates Cdc42-induced Rac activation by means of STEF/Tiam1, and that this process seems to be required for the establishment of neuronal polarity.

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  38. CRMP-2 regulates polarized Numb-mediated endocytosis for axon growth Reviewed

    T Nishimura, Y Fukata, K Kato, T Yamaguchi, Y Matsuura, H Kamiguchi, K Kaibuchi

    NATURE CELL BIOLOGY   Vol. 5 ( 9 ) page: 819 - 826   2003.9

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    Axon growth during neural development is highly dependent on both cytoskeletal re-organization and polarized membrane trafficking. Previously, we demonstrated that collapsin response mediator protein-2 (CRMP-2) is critical for specifying axon/dendrite fate and axon growth in cultured hippocampal neurons, possibly by interacting with tubulin heterodimers and promoting microtubule assembly. Here, we identify Numb as a CRMP-2-interacting protein. Numb has been shown to interact with alpha-adaptin and to be involved in endocytosis. We found that Numb was associated with L1, a neuronal cell adhesion molecule that is endocytosed and recycled at the growth cone, where CRMP-2 and Numb were colocalized. Furthermore, expression of dominant-negative CRMP-2 mutants or knockdown of CRMP-2 message with small-interfering (si) RNA inhibited endocytosis of L1 at axonal growth cones and suppressed axon growth. These results suggest that in addition to regulating microtubule assembly, CRMP-2 is involved in polarized Numb-mediated endocytosis of proteins such as L1.

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▼display all

MISC 75

  1. 【線維化 慢性疾患のキープロセス 多彩な間質細胞が織りなす組織リモデリング"fibrosis"の理解】(第1章)線維芽細胞の多様性 血管周囲に存在する線維芽細胞 Invited

    加藤 勝洋

    実験医学   Vol. 38 ( 12 ) page: 2000 - 2006   2020.8

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    線維化の過程においては、外部からのさまざまな組織の障害によって活性化された線維芽細胞によって、コラーゲンなどの細胞外マトリクスや種々のシグナル分子が分泌される。近年、組織特異的な細胞集団、分子機序によって線維化が起こることがわかってきた。また、線維芽細胞にも多様性が存在し、その一部の集団が線維化に関与すること、その多くは血管近傍に存在していることがわかってきた。しかしながら、特異的にその細胞集団を規定するマーカーの報告は少なく、その細胞の起源や機能、性質などについて不明な点が多い。本稿では、ペリサイトと線維芽細胞の相違について概略を述べ、いくつかの細胞系譜解析から得られた最近の知見をもとに血管周囲に存在する線維芽細胞の線維化への関与について概説する。(著者抄録)

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  2. 臓器特異的なペリサイトの機能解析

    加藤 勝洋

    日本応用酵素協会誌   ( 54 ) page: 85 - 85   2020.3

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  3. 【血管新生-基礎と臨床】臓器・疾患特異的血管新生 肺血管由来アンジオクライン因子を介した恒常性維持機構 Invited

    加藤 勝洋

    医学のあゆみ   Vol. 270 ( 1 ) page: 87 - 93   2019.7

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    血管は全身に血液を供給する点で組織の恒常性維持に必要不可欠の器官である。その一方で、血管自体からのアンジオクライン因子も恒常性の維持に重要な役割を果たすことがわかってきた。また、肺毛細血管は効率的にガス交換を行うために特徴的な形態をしているが、特異的なアンジオクライン因子も発現している。最近、各臓器における血管ネットワークの差異や臓器内での血管細胞の多様性が注目されている。本稿では、肺毛細血管網の特徴を著者らの研究成果を踏まえ、とくにアンジオクラインシグナル、ペリサイトに焦点を当て概説する。(著者抄録)

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    Other Link: https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2019&ichushi_jid=J00060&link_issn=&doc_id=20190708020013&doc_link_id=%2Faa7ayuma%2F2019%2F027001%2F014%2F0087-0093%26dl%3D0&url=http%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Faa7ayuma%2F2019%2F027001%2F014%2F0087-0093%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  4. ERK2-Mediated Phosphorylation of Par3 Regulates Neuronal Polarization

    Yasuhiro Funahashi, Takashi Namba, Shin Fujisue, Norimichi Itoh, Shinichi Nakamuta, Katsuhiro Kato, Akiko Shimada, Chundi Xu, Tomoki Nishioka, Kozo Kaibuchi

    JOURNAL OF PHARMACOLOGICAL SCIENCES   Vol. 124   page: 179P - 179P   2014

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  5. 血管径を規定する分子メカニズムの解明

    加藤 勝洋

    日本応用酵素協会誌   ( 47 ) page: 93 - 93   2013.3

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  6. Cooperative regulation of cellular contractility by Rho-kinase/Scrib/Shroom2 complex

    Tomonari Hamaguchi, Kei Kozawa, Katsuhiro Kato, Shohag Md Hasanuzzaman, Xinjian Zhang, Tomoki Nishioka, Mutsuki Amano, Kozo Kaibuchi

    JOURNAL OF PHARMACOLOGICAL SCIENCES   Vol. 121   page: 71P - 71P   2013

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  7. 【分子標的薬-がんから他疾患までの治癒をめざして-】基礎研究 分子標的薬の作用機序・薬理作用 がん関連標的分子・標的経路 その他のsmall Gタンパクとそのeffector分子群

    加藤 勝洋, 天野 睦紀, 貝淵 弘三

    日本臨床   Vol. 70 ( 増刊8 分子標的薬 ) page: 67 - 70   2012.11

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  8. イノシトール5-ホスファターゼSHIP2はRhoAの新規エフェクターであり、細胞極性や細胞移動に関与する(The inositol 5-phosphatase SHIP2 is a novel effector of RhoA and involved in cell polarity and migration)

    加藤 勝洋

    日本応用酵素協会誌   ( 46 ) page: 111 - 112   2012.2

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  9. Cooperative regulation of cellular contractility by Rho-kinase/Scrib/Shroom2 complex.

    K. Kozawa, K. Kato, T. Hamaguchi, S. M. Hasanuzzaman, X. Zhang, T. Nishioka, M. Amano, K. Kaibuchi

    MOLECULAR BIOLOGY OF THE CELL   Vol. 23   2012

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  10. Rho/Rho-キナーゼシグナルの発見と関連疾患の病態解明

    加藤 勝洋, 天野 睦紀, 貝淵 弘三

    現代医学   Vol. 59 ( 2 ) page: 261 - 270   2011.12

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    従来、血管平滑筋の収縮は、カルシウムシグナルによるミオシン軽鎖のリン酸化で説明されてきたが、カルシウムシグナル以外の制御機構として低分子量GTP結合タンパク質Rhoとその標的分子であるRho-キナーゼの経路が同定された。その後、Rho-キナーゼの特異的な阻害薬を用いることで、Rho-キナーゼが冠動脈攣縮やくも膜下出血後の脳血管攣縮における血管過収縮状態などさまざまな病態に関与していることが示されてきた。昨今では、平滑筋収縮を伴う疾患のみならず、動脈硬化や心血管疾患以外の疾患へのRho-キナーゼの関与が報告されており、Rho-キナーゼ阻害薬が種々の疾患の創薬ターゲットとして注目されている。(著者抄録)

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  11. 【呼吸器と循環器のクロストーク-薬物の進歩-】基礎医学とのダイアローグ Rho-キナーゼ/ROCKと肺高血圧症

    加藤 勝洋, 天野 睦紀, 貝淵 弘三

    THE LUNG-perspectives   Vol. 19 ( 4 ) page: 513 - 517   2011.11

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    血管平滑筋の収縮弛緩のメカニズムは、カルシウムシグナルによるミオシン軽鎖のリン酸化で説明されてきたが、カルシウムシグナル以外の制御機構として低分子量GTP結合タンパク質Rhoとその標的分子であるRho-キナーゼの経路が同定された。その後、Rho-キナーゼの特異的な阻害薬を用いることで、Rho-キナーゼが冠動脈攣縮や脳血管攣縮の血管過収縮状態などさまざまな病態に関与していることが示されてきた。昨今では、肺高血圧症においても、このRho-キナーゼの関与が明らかとなり、Rho-キナーゼ阻害薬が新たな肺高血圧症(PH)の治療薬として注目を集めている。本稿では、PHにおけるRho-キナーゼ依存性病態メカニズムについて概説し、その阻害薬のPH治療薬としての可能性について言及していく。(著者抄録)

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  12. プロテオーム解析を用いた、RhoA新規結合タンパク質の探索

    加藤 勝洋

    日本応用酵素協会誌   ( 45 ) page: 113 - 113   2011.2

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  13. プロテオーム解析を用いた新規RhoA標的蛋白質の探索(Proteomic analysis reveals novel binding partners of active RhoA)

    加藤 勝洋, 矢澤 翼, 森 和孝, 天野 睦紀, 室原 豊明, 貝淵 弘三

    日本細胞生物学会大会講演要旨集   Vol. 62回   page: 173 - 173   2010.5

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  14. 血球特異的RhoファミリーGTP結合タンパク質RhoH新規エフェクター探索

    高須 万里奈, 勝見 章, 加藤 勝洋, 天野 睦紀, 石川 和宏, 金田 典雄, 貝淵 弘三, 直江 知樹

    日本薬学会年会要旨集   Vol. 130年会 ( 3 ) page: 148 - 148   2010.3

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  15. プロテオーム解析を用いた新規RhoA結合蛋白質の探索(Proteomic analysis reveals novel binding partners of activated RhoA)

    加藤 勝洋, 矢澤 翼, 森 和孝, 天野 睦紀, 室原 豊明, 貝淵 弘三

    日本生化学会大会プログラム・講演要旨集   Vol. 82回   page: 4P - 340   2009.9

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  16. 心臓におけるRhoAの新しい結合パートナーのプロテオーム解析による解明(Proteomic analysis reveals novel binding partners of RhoA in heart)

    矢澤 翼, 加藤 勝洋, 森 和孝, 津村 勇多, 天野 睦紀, 室原 豊明, 貝淵 弘三

    日本細胞生物学会大会講演要旨集   Vol. 61回   page: 184 - 184   2009.5

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  17. Rho-kinaseはp190A RhoGAPをリン酸化することによってRhoAの持続的活性化を維持する(Rho-kinase Contributes to Sustained RhoA Activation through Phosphorylation of p190A RhoGAP)

    瀧 健太朗, 森 和孝, 天野 睦紀, 加藤 勝洋, 室原 豊明, 貝淵 弘三

    日本細胞生物学会大会講演要旨集   Vol. 61回   page: 213 - 213   2009.5

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  18. NOVEL MECHANISM OF SUSTAINED RHOA ACTIVATION IN VASCULAR SMOOTH MUSCLE; ITS POSSIBLE ROLE IN VASOSPASM

    Katsuhiro Kato, Kazutaka Mori, Mutsuki Amano, Mikito Takefuji, Toyoaki Murohara, Kozo Kaibuchi

    JOURNAL OF VASCULAR RESEARCH   Vol. 46   page: 14 - 14   2009

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  19. 生前に診断しえた心アミロイドーシスの3例

    高橋 光太, 味岡 正純, 浅野 博, 中島 義仁, 長内 宏之, 横井 健一郎, 植村 祐介, 加藤 勝洋, 神原 貴博, 青山 盛彦, 浅井 裕充, 藤川 裕介, 北川 章充, 中野 嘉久, 酒井 和好

    Circulation Journal   Vol. 72 ( Suppl.II ) page: 926 - 926   2008.4

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  20. 早期CPRの開始と蘇生法としてPCPSを使用することで良好な神経学的予後を得た一例

    神原 貴博, 酒井 和好, 味岡 正純, 浅野 博, 中島 義仁, 長内 宏之, 横井 健一郎, 植村 祐介, 加藤 勝洋

    Circulation Journal   Vol. 72 ( Suppl.II ) page: 928 - 928   2008.4

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  21. 生前に組織診断しえた心臓原発悪性リンパ腫の一例

    植村 祐介, 味岡 正純, 浅野 博, 中島 義仁, 長内 宏之, 横井 健一郎, 横井 清, 加藤 勝洋, 神原 貴博

    Circulation Journal   Vol. 72 ( Suppl.II ) page: 920 - 920   2008.4

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  22. 当院における急性大動脈解離と急性期血流障害の検討

    藤川 裕介, 味岡 正純, 浅野 博, 中島 義仁, 長内 宏之, 横井 健一郎, 植村 祐介, 加藤 勝洋, 神原 貴博, 青山 盛彦, 浅井 裕充, 高橋 光太, 北川 章充, 中野 嘉久, 酒井 和好

    Circulation Journal   Vol. 72 ( Suppl.II ) page: 928 - 928   2008.4

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  23. 当院におけるCRTの有効性の検討

    北川 章充, 味岡 正純, 浅野 博, 中島 義仁, 長内 宏之, 横井 健一郎, 植村 祐介, 加藤 勝洋, 神原 貴博, 青山 盛彦, 浅井 裕充, 高橋 光太, 藤川 裕介, 中野 嘉久, 酒井 和好

    Circulation Journal   Vol. 72 ( Suppl.II ) page: 922 - 922   2008.4

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  24. 当院におけるたこつぼ心筋症例の検討

    青山 盛彦, 味岡 正純, 浅野 博, 中島 義仁, 長内 宏之, 横井 健一郎, 植村 祐介, 加藤 勝洋, 神原 貴博, 浅井 裕充, 高橋 光太, 藤川 裕介, 北川 章充

    Circulation Journal   Vol. 72 ( Suppl.II ) page: 933 - 933   2008.4

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  25. 当院における冠動脈MDCTの現状

    加藤 勝洋, 味岡 正純, 青山 盛彦, 植村 祐介, 神原 貴博, 横井 健一郎, 長内 宏之, 中島 義仁, 浅野 博, 酒井 和好

    Circulation Journal   Vol. 72 ( Suppl.II ) page: 920 - 920   2008.4

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  26. MDCTで見た冠動脈起始異常症の頻度

    中野 嘉久, 味岡 正純, 浅野 博, 中島 義仁, 長内 宏之, 横井 健一郎, 植村 祐介, 加藤 勝洋, 神原 貴博, 青山 盛彦, 浅井 裕充, 高橋 光太, 藤川 裕介, 北川 章充, 酒井 和好

    Circulation Journal   Vol. 72 ( Suppl.II ) page: 920 - 920   2008.4

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  27. 64列マルチスライスCTにて心筋梗塞発症直前の不安定病変を確認しえた1例

    浅井 裕充, 味岡 正純, 浅野 博, 中島 義仁, 長内 宏之, 横井 健一郎, 植村 祐介, 加藤 勝洋, 神原 貴博, 高橋 光太, 藤川 裕介, 北川 章充, 中野 嘉久, 酒井 和好

    Circulation Journal   Vol. 72 ( Suppl.II ) page: 919 - 919   2008.4

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  28. 消化管出血を契機に2箇所のステント血栓症を来たした1症例

    浅井 裕充, 味岡 正純, 藤川 裕介, 青山 盛彦, 植村 祐介, 加藤 勝洋, 神原 貴博, 横井 健一郎, 長内 宏之, 中島 義仁, 浅野 博, 酒井 和好

    Circulation Journal   Vol. 71 ( Suppl.III ) page: 1029 - 1029   2007.10

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  29. 急性大動脈解離急性期血流障害に対してステント留置した2症例

    藤川 裕介, 味岡 正純, 浅井 裕充, 青山 盛彦, 植村 祐介, 加藤 勝洋, 神原 貴博, 横井 健一郎, 長内 宏之, 中島 義仁, 浅野 博, 酒井 和好

    Circulation Journal   Vol. 71 ( Suppl.III ) page: 1021 - 1021   2007.10

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  30. 超高齢者におけるIABPを要した急性心筋梗塞の検討

    浅野 博, 酒井 和好, 味岡 正純, 中島 義仁, 長内 宏之, 横井 健一郎, 植村 祐介, 加藤 勝洋, 神原 貴博

    Journal of Cardiology   Vol. 50 ( Suppl.I ) page: 559 - 559   2007.8

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  31. 急性冠症候群における配偶者の有無について

    青山 盛彦, 植村 祐介, 加藤 勝洋, 神原 貴博, 横井 健一郎, 中谷 理絵, 長内 宏之, 中島 義仁, 浅野 博, 味岡 正純

    Circulation Journal   Vol. 71 ( Suppl.II ) page: 829 - 829   2007.4

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  32. 心タンポナーデを来たしたSLEの一例

    植村 祐介, 味岡 正純, 浅野 博, 中島 義仁, 長内 宏之, 中谷 理絵, 横井 健一郎, 神原 貴博, 加藤 勝洋, 酒井 和好

    Circulation Journal   Vol. 71 ( Suppl.II ) page: 835 - 835   2007.4

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  33. BNP異常低値を示した心不全の1例

    加藤 勝洋, 味岡 正純, 青山 盛彦, 植村 祐介, 神原 貴博, 横井 健一郎, 中谷 理絵, 長内 宏之, 中島 義仁, 浅野 博, 酒井 和好

    Circulation Journal   Vol. 71 ( Suppl.II ) page: 833 - 833   2007.4

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  34. 緊急時における手術適応の同意とインフォームドコンセントの検討

    藤井 恵, 加藤 勝洋, 坂本 和嘉子, 荒木 めぐみ, 味岡 正純, 長谷川 隆一, 川瀬 正樹, 市原 利彦

    日本救急医学会中部地方会誌   Vol. 2   page: 77 - 77   2006.11

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  35. 救急外来胸痛患者におけるD-dimer測定の意義

    坂本 和嘉子, 加藤 勝洋, 荒木 めぐみ, 味岡 正純, 長谷川 隆一, 川瀬 正樹, 市原 利彦

    日本救急医学会中部地方会誌   Vol. 2   page: 73 - 73   2006.11

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  36. Walk inで受診し原因不明な低酸素血症をきたし死亡した1例

    加藤 勝洋, 荒木 めぐみ, 坂本 和嘉子, 味岡 正純, 長谷川 隆一, 川瀬 正樹, 市原 利彦, 岩木 舞

    日本救急医学会中部地方会誌   Vol. 2   page: 84 - 84   2006.11

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  37. 腎機能障害患者の冠動脈造影における重炭酸ナトリウム前投与の腎保護効果

    水野 亮, 味岡 正純, 植村 祐介, 加藤 勝洋, 神原 貴博, 横井 健一郎, 中谷 理絵, 三宅 裕史, 長内 宏之, 中島 義仁, 浅野 博, 酒井 和好

    Circulation Journal   Vol. 70 ( Suppl.III ) page: 1207 - 1207   2006.10

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  38. 当院における慢性完全閉塞病変再開通率の変遷(ストラテジーの選択を中心に)

    神原 貴博, 味岡 正純, 水野 亮, 植村 祐介, 加藤 勝洋, 横井 健一郎, 中谷 理絵, 三宅 裕史, 長内 宏之, 中島 義仁, 浅野 博, 酒井 和好

    Circulation Journal   Vol. 70 ( Suppl.III ) page: 1212 - 1212   2006.10

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  39. 偽性心室頻拍を来し、カテーテルアブレーションを施行した間歇性WPW症候群の一例

    長内 宏之, 味岡 正純, 浅野 博, 中島 義仁, 三宅 裕史, 中谷 理恵, 横井 健一郎, 植村 祐介, 加藤 勝洋, 神原 貴博, 水野 亮, 酒井 和好

    Circulation Journal   Vol. 70 ( Suppl.III ) page: 1206 - 1206   2006.10

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  40. small vesselに対するDESの使用成績

    加藤 勝洋, 味岡 正純, 水野 亮, 植村 祐介, 神原 貴博, 横井 健一郎, 中谷 理絵, 三宅 裕史, 長内 宏之, 中島 義仁, 浅野 博, 酒井 和好

    Circulation Journal   Vol. 70 ( Suppl.III ) page: 1213 - 1213   2006.10

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  41. delivery困難な症例に対して"Rebirth"を用いてCYPHERTMを留置する新しい試み

    植村 祐介, 味岡 正純, 水野 亮, 加藤 勝洋, 神原 貴博, 横井 健一郎, 中谷 理絵, 三宅 裕史, 長内 宏之, 中島 義仁, 浅野 博, 酒井 和好

    Circulation Journal   Vol. 70 ( Suppl.III ) page: 1214 - 1214   2006.10

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  42. CRTへのup gradeが有効であった連合弁膜症による心不全の一例

    長内 宏之, 味岡 正純, 浅野 博, 中島 義仁, 三宅 裕史, 中谷 理恵, 横井 健一郎, 植村 祐介, 加藤 勝洋, 神原 貴博, 水野 亮, 酒井 和好

    Circulation Journal   Vol. 70 ( Suppl.III ) page: 1207 - 1207   2006.10

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  43. CYPHERTM留置後4ヵ月にて再閉塞から心原性ショックに陥った透析患者の1剖検例

    横井 健一郎, 味岡 正純, 水野 亮, 植村 祐介, 加藤 勝洋, 神原 貴博, 中谷 理絵, 三宅 裕史, 長内 宏之, 中島 義仁, 浅野 博, 酒井 和好

    Circulation Journal   Vol. 70 ( Suppl.III ) page: 1213 - 1213   2006.10

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  44. 高齢者(80歳上)緊急開心術症例の検討

    高橋 光太, 市原 利彦, 川瀬 正樹, 長谷川 隆一, 味岡 正純, 中島 義仁, 加藤 勝洋

    日本救急医学会雑誌   Vol. 17 ( 8 ) page: 478 - 478   2006.8

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  45. 心原性ショックにおけるバゾプレシンの使用状況とその有用性

    加藤 勝洋, 植村 祐介, 中島 義仁, 長谷川 隆一, 川瀬 正樹, 市原 利彦, 味岡 正純

    日本救急医学会雑誌   Vol. 17 ( 8 ) page: 439 - 439   2006.8

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  46. 救命できなかった多発外傷における多発外傷の検討 症例から学ぶ反省

    藤井 恵, 市原 利彦, 川瀬 正樹, 長谷川 隆一, 味岡 正純, 中島 義仁, 加藤 勝洋

    日本救急医学会雑誌   Vol. 17 ( 8 ) page: 521 - 521   2006.8

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  47. 新臨床研修システム導入後の救急医療教育における現場の実際と問題点

    市原 利彦, 川瀬 正樹, 加藤 勝洋, 長谷川 隆一, 味岡 正純, 中島 義仁

    日本救急医学会雑誌   Vol. 17 ( 8 ) page: 486 - 486   2006.8

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  48. 病院前医療体制の二次救急病院での取り組み 少しでもpreventable deathをなくす努力

    大江 真由香, 市原 利彦, 川瀬 正樹, 加藤 勝洋, 長谷川 隆一, 味岡 正純, 中島 義仁

    日本救急医学会雑誌   Vol. 17 ( 8 ) page: 450 - 450   2006.8

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  49. 破裂性腹部大動脈瘤の検討 救急医療における救命可能な接点

    永井 美玲, 市原 利彦, 川瀬 正樹, 長谷川 隆一, 味岡 正純, 中島 義仁, 加藤 勝洋

    日本救急医学会雑誌   Vol. 17 ( 8 ) page: 545 - 545   2006.8

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  50. 呼吸停止後ERで心嚢ドレナージにて独歩退院できたStanford A型大動脈解離の1例

    中村 仁美, 市原 利彦, 川瀬 正樹, 長谷川 隆一, 味岡 正純, 中島 義仁, 加藤 勝洋

    日本救急医学会雑誌   Vol. 17 ( 8 ) page: 545 - 545   2006.8

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  51. 2次救急病院における臨床研修教育の工夫及び救急外来のシステム改革 各科相乗り型からER型へ向けての発進

    加藤 勝洋, 中島 義仁, 長谷川 隆一, 川瀬 正樹, 市原 利彦, 味岡 正純

    日本救急医学会雑誌   Vol. 17 ( 8 ) page: 512 - 512   2006.8

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  52. 転落外傷にて搬送されたショックを伴った大動脈解離の1例-救急事前管制による救急医と救急隊員の注意点

    貝沼 慎吾, 市原 利彦, 加藤 勝洋, 長谷川 隆一, 川瀬 正樹, 奥田 美津子, 藤井 恵, 中島 義弘, 味岡 正純

    日本臨床救急医学会雑誌   Vol. 9 ( 2 ) page: 152 - 152   2006.4

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  53. 救急領域における肺血栓塞栓症の検討

    市原 利彦, 川瀬 正樹, 加藤 勝洋, 長谷川 隆一, 奥田 美津子, 藤井 恵, 貝沼 慎吾, 中島 義弘, 味岡 正純

    日本臨床救急医学会雑誌   Vol. 9 ( 2 ) page: 156 - 156   2006.4

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  54. 大規模災害への対応 国際万国博覧会を経験して得た二次救急病院の変化 mass gatheringにおける体制作りとその実際

    加藤 勝洋, 市原 利彦, 川瀬 正樹, 長谷川 隆一, 奥田 美津子, 藤井 恵, 貝沼 慎吾, 中島 義弘, 味岡 正純

    日本臨床救急医学会雑誌   Vol. 9 ( 2 ) page: 112 - 112   2006.4

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  55. 大血管救急疾患におけるD-dimer測定の意義

    奥田 美津子, 市原 利彦, 加藤 勝洋, 長谷川 隆一, 川瀬 正樹, 藤井 恵, 貝沼 慎吾, 中島 義弘, 味岡 正純

    日本臨床救急医学会雑誌   Vol. 9 ( 2 ) page: 153 - 153   2006.4

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  56. イベント会場内応急診療所から紹介された救急疾患のピットフォール-軽症例から潜在する重症病態の留意点

    藤井 恵, 市原 利彦, 加藤 勝洋, 長谷川 隆一, 川瀬 正樹, 奥田 美津子, 貝沼 慎吾, 中島 義弘, 味岡 正純

    日本臨床救急医学会雑誌   Vol. 9 ( 2 ) page: 216 - 216   2006.4

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  57. JPTEC 今後の展開 二次救急病院におけるJPTEC普及の現状と必要性

    市原 利彦, 川瀬 正樹, 加藤 勝洋, 長谷川 隆一, 奥田 美津子, 藤井 恵, 貝沼 慎吾, 中島 義弘, 味岡 正純

    日本臨床救急医学会雑誌   Vol. 9 ( 2 ) page: 124 - 124   2006.4

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  58. 立ちくらみと腹痛で救急搬送されたStanford A型急性大動脈解離と巨大腹部大動脈瘤の管理と治療方針

    加藤 勝洋, 市原 利彦, 川瀬 正樹, 長谷川 隆一, 上田 裕一

    日本集中治療医学会雑誌   Vol. 13 ( Suppl. ) page: 206 - 206   2006.1

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  59. 当院ICUにおけるバソプレシン(VP)の使用状況とその有用性

    植村 祐介, 川瀬 正樹, 長谷川 隆一, 味岡 正純, 市原 利彦, 加藤 勝洋

    日本集中治療医学会雑誌   Vol. 13 ( Suppl. ) page: 188 - 188   2006.1

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  60. 二次救急病院における国際万国博覧会からの疾患の特徴 軽症からの警告症例も参考に

    坂本 和嘉子, 加藤 勝洋, 市原 利彦

    日本集団災害医学会誌   Vol. 10 ( 2 ) page: 190 - 190   2006.1

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  61. 国博覧会を経験して得た実績と二次病院の役割-メディカルコントロール体制における救急診療部の使命

    加藤 勝洋, 坂本 和嘉子, 市原 利彦

    日本集団災害医学会誌   Vol. 10 ( 2 ) page: 189 - 189   2006.1

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  62. ショック状態高度アシドーシスで搬送された右房内浮遊血栓,肺血栓塞栓症の1救命例

    井上 摂理, 市原 利彦, 加藤 勝洋, 長谷川 隆一, 川瀬 正樹, 上田 裕一

    日本集中治療医学会雑誌   Vol. 13 ( Suppl. ) page: 216 - 216   2006.1

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  63. 頸椎骨折および左大腿骨骨幹部骨折をきたし脂肪塞栓症を併発しPCPSを使用して救命し得た1例

    加藤 勝洋, 市原 利彦

    日本外傷学会雑誌   Vol. 19 ( 2 ) page: 190 - 190   2005.4

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  64. 日常外来でのCPR後の救命例 AEDの普及・啓蒙・教育を含め

    高見 悠子, 市原 利彦, 坂本 和嘉子, 加藤 勝洋

    日本臨床救急医学会雑誌   Vol. 8 ( 2 ) page: 113 - 113   2005.4

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  65. 術前脳血管障害を有した胸部大動脈瘤緊急手術例における適応の検討

    加藤 勝洋, 市原 利彦, 坂本 和嘉子

    日本臨床救急医学会雑誌   Vol. 8 ( 2 ) page: 133 - 133   2005.4

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  66. 転落による多発外傷で,呼吸不全が遷延した1例

    貝沼 慎吾, 加藤 崇子, 加藤 勝洋, 市原 利彦, 丹羽 雄大

    日本外傷学会雑誌   Vol. 19 ( 2 ) page: 192 - 192   2005.4

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  67. 多発外傷で腎不全に陥った症例の1救命例 手術適応から見た優先順位の考察

    加藤 崇子, 市原 利彦, 加藤 勝洋

    日本外傷学会雑誌   Vol. 19 ( 2 ) page: 191 - 191   2005.4

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  68. 二次病院における重症胸部外傷の検討

    市原 利彦, 加藤 勝洋

    日本外傷学会雑誌   Vol. 19 ( 2 ) page: 160 - 160   2005.4

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  69. 博覧会開催時における地域基幹病院での災害医療の体制作り 災害拠点病院でない施設の役割と教育

    市原 利彦, 坂本 和嘉子, 加藤 勝洋

    日本臨床救急医学会雑誌   Vol. 8 ( 2 ) page: 103 - 103   2005.4

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  70. 喀血で発症した高度肺機能障害を伴った胸部大動脈肺内穿破に対するステントグラフトの経験

    坂本 和嘉子, 市原 利彦, 加藤 勝洋

    日本臨床救急医学会雑誌   Vol. 8 ( 2 ) page: 133 - 133   2005.4

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  71. 【脳・神経研究2004 神経発生・可塑性と高次脳機能のメカニズム,そして脳・神経疾患の分子機構の解明へ】神経系の発生・分化と回路形成 神経細胞の極性形成機構

    西村 隆史, 山口 知也, 加藤 勝洋, 貝淵 弘三

    実験医学   Vol. 21 ( 17 ) page: 2324 - 2329   2003.11

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    発生時,神経上皮細胞から生み出された神経細胞の多くは脳内を移動し,通常1本の軸索と複数の樹状突起を伸ばし,定められた神経細胞と接続する.神経細胞の基本機能であるシグナルの受け取りと他の細胞への伝達は,神経細胞のもつ極性が重要な役割を果たす.最近,神経細胞の極性形成,つまり軸索と樹状突起の形成には細胞膜輸送や細胞骨格の再構築,更にそれらを制御するシグナル伝達系が重要であることがわかってきた.神経細胞の極性形成における分子メカニズムについて最近の知見をふまえて概説した

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  72. 神経細胞極性制御分子CRMP-2はNumbを介したエンドサイトーシスに関与する

    西村 隆史, 加藤 勝洋, 山口 知也, 深田 優子, 貝淵 弘三

    細胞工学   Vol. 22 ( 11 ) page: 1210 - 1211   2003.10

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  73. 細胞極性形成分子PAR-3の神経細胞における機能及び局在化機構の解析

    加藤 勝洋, 西村 隆史, 深田 優子, 大野 茂男, 貝淵 弘三

    日本細胞生物学会大会講演要旨集   Vol. 56回   page: 48 - 48   2003.5

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  74. Involvement of CRMP-2 on endocytosis and neurite growth through the interaction with Numb

    T Nishimura, Y Fukata, K Kato, Y Matsuura, H Kamiguchi, K Kaibuchi

    MOLECULAR BIOLOGY OF THE CELL   Vol. 13   page: 391A - 391A   2002.11

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    Web of Science

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  75. 細胞極性形成分子ASIP結合タンパク質の同定

    加藤 勝洋, 西村 隆史, 則竹 淳, 中川 誠人, 深田 優子, 深田 正紀, 大野 茂男, 貝淵 弘三

    日本細胞生物学会大会講演要旨集   Vol. 54回   page: 93 - 93   2001.5

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Presentations 10

  1. Working Abroad: lesson from Ralf Adams lab in Germany Invited International conference

    Katsuhiro Kato

    2022.3.5 

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    Event date: 2022.3

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Country:Japan  

  2. 細胞外微粒子と動脈硬化症 International conference

    第7回血管生物医学会若手研究会  2022.3.4  血管生物医学会

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    Event date: 2022.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:兵庫県淡路市   Country:Japan  

  3. Working Abroad: Case Study of a Cardiologist in Germany Invited

    Katsuhiro Kato

    2021.3.27 

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    Event date: 2021.3

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Country:Japan  

  4. Physiology and Pathology of Pulmonary Vasculature Invited

    Katsuhiro Kato

    2021.3.26 

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    Event date: 2021.3

    Language:English   Presentation type:Oral presentation (invited, special)  

    Country:Japan  

  5. Organotypic development of pulmonary vasculature Invited

    Katsuhiro Kato

    2021.3.13 

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    Event date: 2021.3

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Country:Japan  

  6. Organotypic function of pulmonary pericytes.

    Katsuhiro Kato

    2020.12.4 

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    Event date: 2020.12

    Language:English   Presentation type:Symposium, workshop panel (nominated)  

    Country:Japan  

  7. 臓器特異的な血管網と血管形成

    加藤勝洋

    第6回血管生物医学会若手研究会  2020.11.20 

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    Event date: 2020.11

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  8. 肺ペリサイトの臓器特異的な機能 International coauthorship

    第27回日本血管生物医学会学術集会  2019.12.15 

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    Event date: 2019.12

    Language:Japanese   Presentation type:Oral presentation (general)  

    Country:Japan  

  9. Organotypic function of pulmonary pericytes International coauthorship International conference

    Katsuhiro Kato

    Gordon Research Conference on Endothelial Cell Phenotypes in Health and Disease  2018.7.18 

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    Event date: 2018.7

    Language:English   Presentation type:Poster presentation  

    Country:Italy  

  10. Pulmonary pericytes regulate lung morphogenesis International coauthorship International conference

    Katsuhiro Kato

    Keystone Symposia, Vascular Biology and Human Diseases  2018.2.28 

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    Event date: 2018.2 - 2018.3

    Language:English   Presentation type:Oral presentation (invited, special)  

    Country:United States  

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Research Project for Joint Research, Competitive Funding, etc. 11

  1. 肺高血圧症における細動脈内皮細胞機能不全の網羅的解析と創薬に向けた基盤研究

    2020.8

    公益財団法人 武田科学振興財団 2020年度 「医学系研究助成」 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\2000000 ( Direct Cost: \2000000 )

  2. 虚血性心血管疾患における血管新生動態の生体内解析                    に関する研究

    2020.4

    伊藤忠兵衛基金 2020年度学術研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\500000 ( Direct Cost: \495000 、 Indirect Cost:\5000 )

  3. 血管周囲細胞由来脂肪細胞の褐色脂肪組織における役割の検討

    2020.4

    小野医学研究財団・研究奨励助成金 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\1000000 ( Direct Cost: \1000000 )

  4. 生体内イメージングを用いた糖尿病による血管新生ダイナミクス障害の解析

    2020.4

    堀科学芸術振興財団 第29回第4部研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\1000000 ( Direct Cost: \1000000 )

  5. 糖尿病による血管新生ダイナミクス障害の生体内解析

    2020.2

    日本心臓財団 令和元年度研究奨励 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\2000000 ( Direct Cost: \1980000 、 Indirect Cost:\20000 )

  6. 肺細動脈内皮細胞を基軸とした肺高血圧症の病態解明研究

    2020.2

    難病医学研究財団・医学研究奨励助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\2000000 ( Direct Cost: \2000000 )

  7. 間葉系幹細胞による血管新生ダイナミクスの解析

    2020.1

    MSD生命科学財団・研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\2000000 ( Direct Cost: \2000000 )

  8. 遺伝子改変マウスを用いた間葉系幹細胞による血管新生ダイナミクスの生体内解析

    2019.12

    鈴木謙三記念医科学応用研究財団・調査研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\2000000 ( Direct Cost: \1980000 、 Indirect Cost:\20000 )

  9. アンジオクライン因子に焦点を当てた肺高血圧症の病態解析

    2019.12

    持田記念医学薬学振興財団・研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\3000000 ( Direct Cost: \3000000 )

  10. 肺細動脈内皮細胞の機能異常に着目した肺高血圧症の病態解明

    2019.11

    GSKジャパン・研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\2000000 ( Direct Cost: \1840000 、 Indirect Cost:\160000 )

  11. 臓器特異的なペリサイトの機能解析

    2019.10

    2019年度 Vascular Biology Innovation に関する研究助成 

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\500000 ( Direct Cost: \500000 )

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KAKENHI (Grants-in-Aid for Scientific Research) 1

  1. 肺細動脈内皮細胞に着目した肺高血圧症に対する新規治療戦略の開発を目指した病態解明

    Grant number:20K17145  2020.4 - 2022.3

    日本学術振興会  科学研究費助成事業 若手研究  若手研究

    加藤 勝洋

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    Authorship:Principal investigator  Grant type:Competitive

    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    肺動脈性肺高血圧症(PAH)は、肺血管拡張療法の開発により患者予後は以前より改善したものの、治療が奏功しない症例も多く、新規治療薬および診断バイオマーカーの開発が急務である。PAHにおいて末梢側の肺細動脈で異常を示すメカニズムは明らかにされておらず、ここへアプローチすることで肺細動脈内皮細胞を標的とした精密医療・診断法の開発につながると考えられる。本研究では、肺高血圧症モデルマウスより肺細動脈内皮細胞を単離し、次世代シークエンスを用いて発現変動遺伝子を網羅的に探索し、培養細胞および疾患モデル動物で検証し、分子基盤を構築することで、診断・治療方法の新たな開発を目指す。

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