Faculty Profiles - MIZUNO, Masashi

Papers - MIZUNO, Masashi

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今月の特集2 補体をめぐる話題注目の補体異常症 C3腎症

金恒秀, 水野正司

臨床検査 Vol. 68 ( 1 ) page： 88 - 92 2024.1

Effectiveness of additional topical antibiotics for recurrent or refractory exit-site infection: a case series. Reviewed Open Access

Asai N, Suzuki Y, Asai A, Kinashi H, Kamiya K, Hagita J, Matsuoka N, Kawamura S, Fukui S, Kim H, Yamaguchi M, Katsuno, T, Mizuno M, Ishimoto T, Ito Y.

Renal Replacement Therapy. Vol. 10 page： 32 2024

Delaying treatment for peritonitis could be related to longer hospitalization in patients on peritoneal dialysis. Reviewed Open Access

Koshitori Y, Takai N, Isomura Y, Hiramatsu T, Suzuki Y, Kim H, Fukui S, Mizuno M.

Renal Replacement Therapy 2024

Pathophysiological Mechanisms of Peritoneal Fibrosis and Peritoneal Membrane Dysfunction in Peritoneal Dialysis. Invited Reviewed Open Access

2024

特集補体revisited--抗補体療法はどこまで進んだか? 非典型溶血性尿毒症症候群 Invited

水野正司

医学のあゆみ Vol. 287 ( 10 ) page： 757 - 761 2023.12

遺伝性血管性浮腫(Hereditary angioedema:HAE)診療ガイドライン改訂2023年版

堀内孝彦, 大澤勲, 宮田敏行, 赤津裕康, 今井優樹, 大谷克城, 奥健志, 関根英治, 塚本浩, 中尾実樹, 西村純一, 水野正司, 村上良子, 井上徳光, 一般社団法人日本補体学会HAEガイドライン作成委員会

補体 Vol. 60 ( 1 ) page： 23 - 23 2023.8

学校検尿でみつかった、電顕像にて電子密度の異なる沈着物を認めるDense Deposit Diseaseの13歳女児例

手塚優子, 新野亮治, 木内拓海, 岡本健太郎, 村上至孝, 松田修, 澤井俊宏, 水野正司, 清水章

日本小児腎臓病学会雑誌 Vol. 36 ( Suppl. ) page： 179 - 179 2023.5

Inhibition of Transglutaminase 2 Reduces Peritoneal Injury in a Chlorhexidine-Induced Peritoneal Fibrosis Model. Reviewed International journal

Shunnosuke Kunoki, Hideki Tatsukawa, Yukinao Sakai, Hiroshi Kinashi, Tetsuyoshi Kariya, Yasuhiro Suzuki, Masashi Mizuno, Makoto Yamaguchi, Hiroyuki Sasakura, Masashi Ikeno, Kosei Takeuchi, Takuji Ishimoto, Kiyotaka Hitomi, Yasuhiko Ito

Laboratory investigation; a journal of technical methods and pathology Vol. 103 ( 4 ) page： 100050 - 100050 2023.4

Language：English Publishing type：Research paper (scientific journal)

Long-term peritoneal dialysis (PD) is often associated with peritoneal dysfunction leading to withdrawal from PD. The characteristic pathologic features of peritoneal dysfunction are widely attributed to peritoneal fibrosis and angiogenesis. The detailed mechanisms remain unclear, and treatment targets in clinical settings have yet to be identified. We investigated transglutaminase 2 (TG2) as a possible novel therapeutic target for peritoneal injury. TG2 and fibrosis, inflammation, and angiogenesis were investigated in a chlorhexidine gluconate (CG)-induced model of peritoneal inflammation and fibrosis, representing a noninfectious model of PD-related peritonitis. Transforming growth factor (TGF)-β type I receptor (TGFβR-I) inhibitor and TG2-knockout mice were used for TGF-β and TG2 inhibition studies, respectively. Double immunostaining was performed to identify cells expressing TG2 and endothelial-mesenchymal transition (EndMT). In the rat CG model of peritoneal fibrosis, in situ TG2 activity and protein expression increased during the development of peritoneal fibrosis, as well as increases in peritoneal thickness and numbers of blood vessels and macrophages. TGFβR-I inhibitor suppressed TG2 activity and protein expression, as well as peritoneal fibrosis and angiogenesis. TGF-β1 expression, peritoneal fibrosis, and angiogenesis were suppressed in TG2-knockout mice. TG2 activity was detected by α-smooth muscle actin-positive myofibroblasts, CD31-positive endothelial cells, and ED-1-positive macrophages. CD31-positive endothelial cells in the CG model were α-smooth muscle actin-positive, vimentin-positive, and vascular endothelial-cadherin-negative, suggesting EndMT. In the CG model, EndMT was suppressed in TG2-knockout mice. TG2 was involved in the interactive regulation of TGF-β. As inhibition of TG2 reduced peritoneal fibrosis, angiogenesis, and inflammation associated with TGF-β and vascular endothelial growth factor-A suppression, TG2 may provide a new therapeutic target for ameliorating peritoneal injuries in PD.

DOI： 10.1016/j.labinv.2022.100050

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Video-assisted thoracoscopic surgery for pleuroperitoneal communication International journal

Tsubouchi, H; Nakamura, S; Fukui, T; Kadomatsu, Y; Ueno, H; Ozeki, N; Fukumoto, K; Mizuno, M; Chen-Yoshikawa, TF

ASIAN JOURNAL OF ENDOSCOPIC SURGERY Vol. 16 ( 2 ) page： 262 - 265 2023.4

Nutritional Assessment and Nutrient Supplement in Patients with Chronic Kidney Disease Open Access

Mizuno, M

NUTRIENTS Vol. 15 ( 8 ) 2023.4

特集 Genetics in CKD 疾患編補体関連遺伝子の異常と腎疾患

金恒秀, 水野正司

腎と透析 Vol. 94 ( 3 ) page： 405 - 410 2023.3

Durvalumab plus carboplatin-etoposide treatment in a patient with small-cell lung cancer on hemodialysis: A case report and literature review. Reviewed Open Access

Ushijima F, Hase T, Yamashita Y, Kim H, Shimokata T, Kondo C, Sato T, Baba T, Watanabe S, Futamura K, Ando Y, Mizuno M, Ishii M.

Int Cancer Conf J. Vol. 13 ( 2 ) page： 88 - 92 2023.2

Case report: Thrombotic microangiopathy concomitant with macrophage activation syndrome in systemic lupus erythematosus refractory to conventional treatment successfully treated with eculizumab International journal Open Access

Makoto Yamaguchi, Masashi Mizuno, Fumiya Kitamura, Shiho Iwagaitsu, Hironobu Nobata, Hiroshi Kinashi, Shogo Banno, Akimasa Asai, Takuji Ishimoto, Takayuki Katsuno, Yasuhiko Ito

Frontiers in Medicine Vol. 9 page： 1097528 2023.1

Language：English Publishing type：Research paper (scientific journal) Publisher：Frontiers Media SA

Thrombotic microangiopathy (TMA) is a rare but life-threatening complication of systemic lupus erythematosus (SLE). Macrophage activation syndrome (MAS) is also a rare, life-threatening hyperinflammatory condition that is comorbid with SLE. However, the association between TMA and MAS in patients with SLE has rarely been assessed, and the difficulty of diagnosing these conditions remains prevalent. The efficacy of eculizumab has been reported for SLE patients whose conditions are complicated with TMA. However, no study has investigated the therapeutic efficacy of eculizumab for TMA concomitant with SLE-associated MAS. Herein, we report the first case of TMA concomitant with SLE-associated MAS that was initially refractory to conventional immunosuppressive therapy but showed remarkable recovery after eculizumab treatment. Furthermore, we evaluated serum syndecan-1 and hyaluronan levels, which are biomarkers of endothelial damage. We found that these levels decreased after the administration of eculizumab, suggesting that TMA was the main pathology of the patient. This case illustrates that it is important to appropriately assess the possibility of TMA during the course of SLE-associated MAS and consider the use of eculizumab as necessary.

DOI： 10.3389/fmed.2022.1097528

Recurrent Cerebrovascular Complications under Enzyme Replacement Therapy in a Patient with Fabry Disease on Peritoneal Dialysis Reviewed International journal Open Access

Muto Reiko, Suzuki Yasuhiro, Shimizu Hideaki, Yasuda Kaoru, Ishimoto Takuji, Maruyama Shoichi, Ito Yasuhiko, Mizuno Masashi

Internal Medicine Vol. 62 ( 3 ) page： 565 - 569 2023

Authorship：Last author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：The Japanese Society of Internal Medicine

Fabry disease is an X-linked lysosomal storage disorder due to mutations in the alpha-galactosidase A gene, which leads to the accumulation of globotriaosylceramide in various organs. In Fabry disease with end-stage renal disease (ESRD), cerebrovascular events are lethal, even with enzyme replacement therapy (ERT). However, the utility of biomarkers to evaluate the ERT response is unclear. We herein report a case of recurrent cerebrovascular complications under ERT in a Fabry disease patient, progressing to ESRD on peritoneal dialysis. Further studies are warranted, but Fabry disease patients with ESRD receiving ERT might need careful long-term follow-up in cases with cerebrovascular manifestations.

DOI： 10.2169/internalmedicine.0185-22

ASSISTED PD：Problems and Countermeasures Based on Home-Visit Nursing Station Surveys Reviewed

Takai Nami, Nakabayashi Kichio, Kawashima Shoichi, Mizuno Masashi, Koide Shigehisa, Kasuga Hirotake, Saka Yosuke, Sakai Emiko, Inaguma Daijo, Ito Yasuhiko

Nihon Toseki Igakkai Zasshi Vol. 56 ( 11 ) page： 401 - 409 2023

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：The Japanese Society for Dialysis Therapy

[Objective] To investigate factors hindering the spread of assisted peritoneal dialysis (PD) to support elderly patients in Japan, a survey of PD acceptance at home nursing stations was administered. [Method] A questionnaire survey was conducted involving 616 home-visit nursing stations in Aichi Prefecture, 368 of which were registered with the Aichi Medical Association or Aichi Council of Home-Visit Nursing Stations. [Results] A total of 132 facilities were surveyed, for a collection rate of 35％. The breakdown was as follows：37 home nursing stations were accepting PD patients, 59 were considering accepting PD patients, and 20 were not considering accepting PD patients. A total of 20％ of the facilities were always involved in PD patient visits. Other facilities had only a few opportunities to see PD patients per year. The most common conditions for acceptance by visiting nurses were："medication management" and "emotional support," followed by "PD-bag exchange" and "exit site care". The most common considerations for acceptance were："preparation of APD cycler" and "monitoring the operation of APD equipment," such as preparation of APD equipment. [Conclusion] In order for home health care nurses, who are key personnel in ASSISTED PD, to be able to accept PD patients without anxiety, collaboration and multidisciplinary cooperation, such as joint visits and sharing of care methods with medical staff at PD treatment facilities, are required.

DOI： 10.4009/jsdt.56.401

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Long-term peritoneal dialysate exposure modulates expression of membrane complement regulators in human peritoneal mesothelial cells Reviewed International journal Open Access

Kobayashi Kazuma, Ozeki Toshikazu, Kim Hangsoo, Imai Masaki, Kojima Hiroshi, Iguchi Daiki, Fukui Sosuke, Suzuki Masafumi, Suzuki Yasuhiro, Maruyama Shoichi, Ito Yasuhiko, Mizuno Masashi

FRONTIERS IN MEDICINE Vol. 9 page： 972592 2022.12

Interleukin-6 blockade reduces salt-induced cardiac inflammation and fibrosis in subtotal nephrectomized mice. Reviewed International journal

Hiroya Tanaka, Ting Sun, Hiroshi Kinashi, Keisuke Kamiya, Makoto Yamaguchi, Hironobu Nobata, Fumiko Sakata, Hangsoo Kim, Masashi Mizuno, Shunnosuke Kunoki, Yukinao Sakai, Akiyoshi Hirayama, Tomoyoshi Soga, Kazuhiro Yoshikawa, Takuji Ishimoto, Yasuhiko Ito

American journal of physiology. Renal physiology Vol. 323 ( 6 ) page： F654 - F665 2022.12

Language：English Publishing type：Research paper (scientific journal)

Cardiovascular disease is the most common comorbidity in chronic kidney disease (CKD) patients, affecting both their prognosis and quality of life. Cardiac fibrosis is common in CKD patients with left ventricular diastolic dysfunction, and it is associated with increased risk of heart failure and mortality. Recent evidence suggests that high salt intake activates immune responses associated with local accumulation of sodium. We reported that high salt intake promotes cardiac inflammation in subtotal nephrectomized (Nx) mice. We investigated the effects of administration of MR16-1, a rat anti-mouse monoclonal interleukin (IL)-6 receptor antibody, in Nx mice with salt loading (Nx-salt). Expression of monocyte chemoattractant protein (MCP)-1, tumor necrosis factor (TNF)-a, IL-1b, and IL-6 mRNAs and macrophage infiltration was significantly reduced in the heart of Nx-salt mice treated with MR16-1 (Nx-salt-MR16-1) as compared with Nx-salt mice treated with control rat immunoglobulin G1 (rat IgG1) (Nx-salt-rat IgG1). Correspondingly, cardiac fibrosis was significantly attenuated in Nx-salt-MR16-1 mice compared with Nx-salt-rat IgG1 mice. Furthermore, in the heart of Nx-salt-MR16-1 mice, expression of mRNA for nicotinamide adenine dinucleotide phosphate oxidase-2, an oxidative stress marker, was significantly downregulated compared with Nx-salt-rat IgG1 mice. Increases in cardiac metabolites including histidine and γ-butyrobetaine were also reversed by IL-6 blockade treatment. In conclusion, IL-6 blockade exerts anti-inflammatory, anti-fibrotic, and partial anti-oxidative effects in the heart of Nx-salt mice.

DOI： 10.1152/ajprenal.00396.2021

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A case of C3 glomerulopathy with nephritis-associated plasmin receptor positivity without a history of streptococcal infection International journal Open Access

Asano, M; Oda, T; Mizuno, M

CEN CASE REPORTS Vol. 11 ( 2 ) page： 259 - 264 2022.5

Expression of a Crry/p65 is reduced in acute lung injury induced by extracellular histones. International journal Open Access

Fumihiko Nagano, Tomohiro Mizuno, Masaki Imai, Kazuo Takahashi, Naotake Tsuboi, Shoichi Maruyama, Masashi Mizuno

FEBS open bio Vol. 12 ( 1 ) page： 192 - 202 2022.1

Language：English Publishing type：Research paper (scientific journal)

Acute lung injury (ALI) occurs in patients with severe sepsis and has a mortality rate of 40%-60%. Severe sepsis promotes the release of histones from dying cells, which can induce platelet aggregation, activate coagulation and cause endothelial cell (EC) death. We previously reported that the expression of membrane complement receptor type 1-related gene Y (Crry)/p65, which plays a principal role in defence against abnormal activation of complement in the blood, is reduced in response to peritoneal mesothelial cell injury, and we hence hypothesized that a similar mechanism occurs in pulmonary ECs. In this study, we examined the role of Crry/p65 in histone-mediated ALI using an experimental animal model. In ALI model mice, exposure to extracellular histones induces lung injury and results in a decrease in Crry/p65 expression. The levels of lactic acid dehydrogenase (LDH), a marker of cell damage, were significantly increased in the serum of ALI model compared with vehicle mice. The significant inverse correlation between the expression of Crry/p65 and LDH levels in plasma revealed an association between Crry/p65 expression and cell damage. The levels of complement component 3a (C3a) were also significantly increased in the serum of the ALI model compared with vehicle mice. Notably, a C3a receptor antagonist ameliorated lung injury induced by histones. We hypothesize that extracellular histones induce complement activation via down-regulation of Crry/p65 and that C3a might serve as a therapeutic target for the treatment of ALI.

DOI： 10.1002/2211-5463.13322

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A novel model mouse for type 2 diabetes mellitus with early onset and persistent hyperglycemia Reviewed International journal

Yoshida Kanta, Ohno Tamio, Mizuno Masashi, Yokoi Norihide, Miyasaka Yuki, Kobayashi Misato, Horio Fumihiko, Ikegami Hiroshi

Experimental Animals Vol. 71 ( 4 ) page： 510 - 518 2022

Language：English Publishing type：Research paper (scientific journal) Publisher：Japanese Association for Laboratory Animal Science

Various mouse models of type 2 diabetes have been established, but few of these show early onset and persistent hyperglycemia. We have established a congenic mouse strain (NSY.B6-Tyr+,Ay) in which a spontaneous mutation of the agouti yellow (Ay) gene, which causes obesity by hyperphagia, was introduced into the NSY strain, which shows increased glucose intolerance with age. This strain has been maintained as a segregating inbred strain by mating obese yellow (Ay/a) males with normal black (a/a) females. All yellow males showed marked obesity and hyperglycemia (mean blood glucose level >400 mg/dl) from 10 to 24 weeks of age. The yellow males also showed glucose intolerance and insulin resistance. They provide a potentially valuable model mouse for research into type 2 diabetes, hyperlipidemia, fatty liver, and renal glomerular complications. Yellow female mice also showed marked obesity, but the incidence of diabetes and the severity of various pathological conditions were milder than in yellow males. None of the black mice showed hyperglycemia in either sex. NSY.B6-Tyr+,Ay strain has good fertility and does not display inter-male aggression, making them useful as a new model for type 2 diabetes with early onset and persistent hyperglycemia.

DOI： 10.1538/expanim.22-0061

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Papers - MIZUNO, Masashi