Faculty Profiles - ARIMA, Hiroshi

Papers - ARIMA, Hiroshi

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Anti-pituitary antibodies as a marker of autoimmunity in pituitary glands.

Iwama S, Arima H

Endocrine journal Vol. 67 ( 11 ) page： 1077 - 1083 2020.11

Endoplasmic reticulum chaperone BiP/GRP78 knockdown leads to autophagy and cell death of arginine vasopressin neurons in mice. Reviewed

Kawaguchi Y, Hagiwara D, Miyata T, Hodai Y, Kurimoto J, Takagi H, Suga H, Kobayashi T, Sugiyama M, Onoue T, Ito Y, Iwama S, Banno R, Grinevich V, Arima H

Scientific reports Vol. 10 ( 1 ) page： 19730 2020.11

Language：English Publishing type：Research paper (scientific journal) Publisher：Springer Science and Business Media LLC

<title>Abstract</title>The immunoglobulin heavy chain binding protein (BiP), also referred to as 78-kDa glucose-regulated protein (GRP78), is a pivotal endoplasmic reticulum (ER) chaperone which modulates the unfolded protein response under ER stress. Our previous studies showed that BiP is expressed in arginine vasopressin (AVP) neurons under non-stress conditions and that BiP expression is upregulated in proportion to the increased AVP expression under dehydration. To clarify the role of BiP in AVP neurons, we used a viral approach in combination with shRNA interference for BiP knockdown in mouse AVP neurons. Injection of a recombinant adeno-associated virus equipped with a mouse AVP promoter and BiP shRNA cassette provided specific BiP knockdown in AVP neurons of the supraoptic (SON) and paraventricular nuclei (PVN) in mice. AVP neuron-specific BiP knockdown led to ER stress and AVP neuronal loss in the SON and PVN, resulting in increased urine volume due to lack of AVP secretion. Immunoelectron microscopy of AVP neurons revealed that autophagy was activated through the process of AVP neuronal loss, whereas no obvious features characteristic of apoptosis were observed. Pharmacological inhibition of autophagy by chloroquine exacerbated the AVP neuronal loss due to BiP knockdown, indicating a protective role of autophagy in AVP neurons under ER stress. In summary, our results demonstrate that BiP is essential for the AVP neuron system.

DOI： 10.1038/s41598-020-76839-z

Web of Science

PubMed

Other Link： http://www.nature.com/articles/s41598-020-76839-z

Degradation of Mutant Protein Aggregates within the Endoplasmic Reticulum of Vasopressin Neurons. Reviewed International journal

Miyata T, Hagiwara D, Hodai Y, Miwata T, Kawaguchi Y, Kurimoto J, Ozaki H, Mitsumoto K, Takagi H, Suga H, Kobayashi T, Sugiyama M, Onoue T, Ito Y, Iwama S, Banno R, Matsumoto M, Kawakami N, Ohno N, Sakamoto H, Arima H

iScience Vol. 23 ( 10 ) page： 101648 - 101648 2020.10

Authorship：Last author,　Corresponding author Language：English Publishing type：Research paper (scientific journal)

Misfolded or unfolded proteins in the ER are said to be degraded only after translocation or isolation from the ER. Here, we describe a mechanism by which mutant proteins are degraded within the ER. Aggregates of mutant arginine vasopressin (AVP) precursor were confined to ER-associated compartments (ERACs) connected to the ER in AVP neurons of a mouse model of familial neurohypophysial diabetes insipidus. The ERACs were enclosed by membranes, an ER chaperone and marker protein of phagophores and autophagosomes were expressed around the aggregates, and lysosomes fused with the ERACs. Moreover, lysosome-related molecules were present within the ERACs, and aggregate degradation within the ERACs was dependent on autophagic-lysosomal activity. Thus, we demonstrate that protein aggregates can be degraded by autophagic-lysosomal machinery within specialized compartments of the ER.

DOI： 10.1016/j.isci.2020.101648

Web of Science

PubMed

Generation of four induced pluripotent stem cell lines (FHUi003-A, FHUi003-B, FHUi004-A and FHUi004-B) from two affected individuals of a familial neurohypophyseal diabetes insipidus family Invited

Yoshida Satoru, Okura Hanayuki, Suga Hidetaka, Soen Mika, Kawaguchi Yohei, Kurimoto Junki, Miyata Takashi, Takagi Hiroshi, Arima Hiroshi, Fujikawa Tatsuya, Otsuka Fumio, Matsuyama Akifumi

STEM CELL RESEARCH Vol. 48 page： 101960 - 101960 2020.10

The Smart Life Stay (SLS) program: effects of a lifestyle intervention program in combination with health tourism and health guidance for type 2 diabetes (vol 10, 33, 2020) Open Access

Matsushita, M; Muramoto, A; Nomura, E; Eguchi, Y; Kato, A; Sano, Y; Kabayama, M; Arakawa, M; Oguma, Y; Yabe, D; Matsunaga, M; Yatsuya, H; Arima, H; Tsushita, K

NUTRITION & DIABETES Vol. 10 ( 1 ) page： 34 2020.9

Higher level of body mass index (≥ 22 kg/m<SUP>2</SUP>) is a useful predictor of non-insulin requirement in Slowly Progressive Insulin-Dependent (Type 1) Diabetes Mellitus (SPIDDM) Reviewed

Onoue, T; Wada, E; Hayase, A; Handa, T; Furukawa, M; Kobayashi, T; Goto, M; Arima, H

DIABETOLOGIA Vol. 63 ( SUPPL 1 ) page： S176 - S176 2020.9

Protein tyrosine phosphatase 1B deficiency enhances leptin action to improve glucose homeostasis in IDDM treatment with leptin

Ito, Y; Banno, R; Sun, R; Yaginuma, H; Taki, K; Sugiyama, M; Tsunekawa, T; Takagi, H; Arima, H

DIABETOLOGIA Vol. 63 ( SUPPL 1 ) page： S12 - S12 2020.9

Peripheral combination treatment of leptin and SGLT2 inhibitor improved glucose metabolism in insulin-dependent diabetes mice Reviewed

Yaginuma, H; Banno, R; Sun, R; Taki, K; Sugiyama, M; Tsunekawa, T; Takagi, H; Ito, Y; Arima, H

DIABETOLOGIA Vol. 63 ( SUPPL 1 ) page： S259 - S260 2020.9

The regulation of glucose metabolism by astrocytes in diet induced obesity mice Reviewed

Sugiyama, M; Banno, R; Sun, R; Yaginuma, H; Taki, K; Takagi, H; Ito, Y; Yamanaka, K; Arima, H

DIABETOLOGIA Vol. 63 ( SUPPL 1 ) page： S266 - S266 2020.9

【糖尿病・内分泌代謝疾患における妊娠と出産】中枢性尿崩症

高木博史, 有馬寛

糖尿病・内分泌代謝科 Vol. 51 ( 3 ) page： 211 - 214 2020.9

The Smart Life Stay (SLS) program: effects of a lifestyle intervention program in combination with health tourism and health guidance for type 2 diabetes Reviewed International journal

Matsushita Madoka, Muramoto Akiko, Nomura Eri, Eguchi Yukari, Kato Ayako, Sano Yoshiko, Kabayama Mai, Arakawa Masashi, Oguma Yuko, Yabe Daisuke, Matsunaga Masaaki, Yatsuya Hiroshi, Arima Hiroshi, Tsushita Kazuyo

NUTRITION & DIABETES Vol. 10 ( 1 ) page： 33 - 33 2020.8

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

BACKGROUND: The aim of this study was to determine the effectiveness of the Smart Life Stay (SLS) program, which is an experience-oriented stayover program, in combination with health tourism and mandatory health guidance on glucose metabolism after 2 years. METHODS: The participants of the SLS program (n = 792) were recruited from a database of 23 medical insurers. They underwent a mandatory health examination termed Specific Health Checkups in 2014. The participants were included if they had diabetes or were at a high risk of diabetes and if they satisfied the following inclusion criteria: (1) body mass index (BMI; kg/m2) > 25, or (2) waist circumference (WC; cm) > 85 for men and > 90 for women, or (3) hemoglobin A1c (HbA1c; %) > 5.6, or (4) fasting plasma glucose (FPG; mg/dl) > 100. Individuals who corresponded to one or more items were included as study participants. The control subjects (n = 3645) were nonparticipants of the program who were selected from the database and met the inclusion criteria. The lifestyle changes and changes in mean BMI, WC, FPG, and HbA1c in both groups from baseline to 2-year follow-up were compared by inverse probability weighting of a propensity score. RESULTS: The percentage of people who exercised regularly increased significantly in the SLS group compared with the control group. In the SLS group, BW, BMI, and WC significantly decreased by 1.75 kg, 0.60 kg/m2, and 1.45 cm, respectively, whereas in the control group, WC, FPG, and HbA1c increased significantly by 0.38 cm, 3.37 mg/dl, and 0.12%, respectively. The comparison between groups revealed that the BW, BMI, WC, FPG, and HbA1c improved significantly in the SLS group. CONCLUSIONS: The SLS program is suggested to help improve glucose metabolism. This program could be a feasible option as a lifestyle intervention program for diabetes.

DOI： 10.1038/s41387-020-00136-x

Web of Science

PubMed

免疫チェックポイント阻害薬による下垂体障害に関連する自己抗体の網羅的解析

奥地剛之, 岩間信太郎, 伊藤雅晃, 岡田則男, 小林朋子, 安田康紀, 有馬寛

日本内分泌学会雑誌 Vol. 96 ( 1 ) page： 245 - 245 2020.8

甲状腺の内部エコー不均一は甲状腺自己抗体陽性者における抗PD-1抗体関連甲状腺障害の高リスクマーカーとなる

岡田則男, 岩間信太郎, 伊藤雅晃, 奥地剛之, 小林朋子, 安田康紀, 有馬寛

日本内分泌学会雑誌 Vol. 96 ( 1 ) page： 243 - 243 2020.8

インスリン依存性糖尿病モデルマウスの糖代謝はインスリン非投与下でレプチンおよびSGLT2阻害剤の併用投与により改善する

柳沼裕史, 坂野僚一, 孫汝楠, 滝啓吾, 杉山摩利子, 恒川卓, 高木博史, 伊藤禎浩, 有馬寛

糖尿病 Vol. 63 ( Suppl.1 ) page： S - 199 2020.8

高脂肪食負荷マウスにおいて食塩過剰摂取はインスリン分泌低下を介して耐糖能を悪化させる

滝啓吾, 高木博史, 孫汝楠, 柳沼裕史, 杉山摩利子, 恒川卓, 伊藤禎浩, 坂野僚一, 有馬寛

糖尿病 Vol. 63 ( Suppl.1 ) page： S - 131 2020.8

報酬系による糖代謝調節機構の解明 GABAB受容体ノックアウトマウスを用いた検討

恒川卓, 坂野僚一, 孫汝楠, 柳沼裕史, 滝啓吾, 杉山摩利子, 高木博史, 伊藤禎浩, 有馬寛

糖尿病 Vol. 63 ( Suppl.1 ) page： S - 111 2020.8

タモキシフェン誘導性Creマウスを用いたアストロサイト特異的PTP1B欠損マウスの表現型解析

杉山摩利子, 坂野僚一, 孫汝楠, 柳沼裕史, 滝啓吾, 恒川卓, 高木博史, 伊藤禎浩, 有馬寛

日本内分泌学会雑誌 Vol. 96 ( 1 ) page： 352 - 352 2020.8

Generation of three induced pluripotent stem cell (iPSC) lines from a multiple endocrine neoplasia type 1 (MEN1) patient and three iPSC lines from an unaffected relative of the patient. Invited Reviewed International journal

Satoru Yoshida, Hanayuki Okura, Hidetaka Suga, Tomohiko Nishitomi, Akihiro Sakurai, Hiroshi Arima, Akifumi Matsuyama

Stem cell research Vol. 46 page： 101846 - 101846 2020.7

Language：English Publishing type：Research paper (scientific journal) Publisher：Elsevier BV

We generated three disease-specific iPSC lines from a Multiple endocrine neoplasia type 1 (MEN1) patient and three control iPSC lines from an unaffected blood relative of the patient using unutilized lymphoblastoid B cell lines (LCLs) as a cell resource. The expression of pluripotency markers, retaining of normal karyotype of chromosome, absence of episomal vectors used for generating the iPSCs and EBV used for generating LCLs, and the potential to differentiate into three germ layers, were confirmed for each iPSC line. These iPSC lines can be useful for construction of the disease models in vitro, and elucidation of the disease mechanisms.

DOI： 10.1016/j.scr.2020.101846

Web of Science

PubMed

Hypothalamic glial cells isolated by MACS reveal that microglia and astrocytes induce hypothalamic inflammation via different processes under high-fat diet conditions Reviewed International journal

Mariko Sugiyama, Ryoichi Banno, Hiroshi Yaginuma, Keigo Taki, Akira Mizoguchi, Taku Tsunekawa, Takeshi Onoue, Hiroshi Takagi, Yoshihiro Ito, Shintaro Iwama, Motomitsu Goto, Hidetaka Suga, Okiru Komine, Koji Yamanaka, Hiroshi Arima

Neurochemistry International Vol. 136 page： 104733 - 104733 2020.6

Authorship：Last author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：Elsevier BV

Glial cells can mediate hypothalamic inflammatory processes induced in response to a high-fat diet (HFD). We used magnetic-activated cell sorting (MACS) to isolate microglia and astrocytes from hypothalamus of mice fed HFD and examined changes in expression of inflammation-related cytokines and markers related to glial cell activation status. Hypothalamus from male C57BL6 mice fed a chow diet (chow) or HFD for 1, 3, or 28 days were collected and microglia and astrocytes were isolated by MACS. After confirming cell viability by fluorescence activated cell sorting, mRNA expression levels of inflammation-related cytokines and markers of glial cell activation status were examined by qRT-PCR, which revealed that both glial cell types isolated by MACS retained specificity. On day 3 of HFD, both CD86 and TNFα mRNA expression was significantly increased in microglia relative to the chow group. In astrocytes, TNFα mRNA expression levels were similar between the chow and HFD groups on day 3, but anti-inflammatory cytokine IL-10 levels were significantly increased. On day 7 of HFD, TNFα expression in microglia decreased to levels comparable to the chow group while that in astrocytes remained unchanged. On day 28 of HFD, TNFα levels were significantly increased in both microglia and astrocytes, which had increased mRNA expression of CD86 and MAO-B, respectively. For both glial cell types, results for TNFα expression assessed by RT-PCR and immunohistochemical analysis were similar. These results indicate that the role of microglia and astrocytes in hypothalamic inflammation under HFD conditions changed with time and these changes were accompanied by changes in the activation status of glial cells. Our data suggest that early after initiating HFD, hypothalamic astrocytes suppress diet-induced inflammation at least in part by secreting IL-10, whereas continued HFD feeding impairs this suppressive function such that both microglia and astrocytes promote hypothalamic inflammation.

DOI： 10.1016/j.neuint.2020.104733

Web of Science

PubMed

Anti-thyroid antibodies and thyroid echo pattern at baseline as risk factors for thyroid dysfunction induced by anti-programmed cell death-1 antibodies: a prospective study. Reviewed International journal

Norio Okada, Shintaro Iwama, Takayuki Okuji, Tomoko Kobayashi, Yoshinori Yasuda, Eri Wada, Takeshi Onoue, Motomitsu Goto, Mariko Sugiyama, Taku Tsunekawa, Hiroshi Takagi, Daisuke Hagiwara, Yoshihiro Ito, Hidetaka Suga, Ryoichi Banno, Tetsunari Hase, Masahiro Morise, Mitsuro Kanda, Kenji Yokota, Naozumi Hashimoto, Masahiko Ando, Yasushi Fujimoto, Masato Nagino, Yasuhiro Kodera, Mitsuhiro Fujishiro, Hideharu Hibi, Michihiko Sone, Hitoshi Kiyoi, Momokazu Gotoh, Yuichi Ando, Masashi Akiyama, Yoshinori Hasegawa, Hiroshi Arima

British journal of cancer Vol. 122 ( 6 ) page： 771 - 777 2020.3

Authorship：Last author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：Springer Science and Business Media LLC

BACKGROUND: Anti-programmed cell death-1 (PD-1) antibodies can cause thyroid dysfunction. However, no predictive biomarkers enabling stratification of thyroid dysfunction risk have been identified. METHODS: A total of 209 patients treated with an anti-PD-1 antibody were evaluated for anti-thyroid antibodies at baseline and prospectively for thyroid function every 6 weeks for 24 weeks after treatment initiation, and then observed until the visits stopped. Thyroid ultrasonography was performed if the patient was positive for anti-thyroid antibodies at baseline. RESULTS: Of the 209 patients, 19 (9.1%) developed thyroid dysfunction (destructive thyroiditis or hypothyroidism). The cumulative incidence of thyroid dysfunction was significantly higher in patients who were positive vs. negative for anti-thyroid antibodies (15/44 [34.1%] vs. 4/165 [2.4%], p < 0.001). Forty-two patients positive for anti-thyroid antibodies at baseline were divided into two groups according to the presence of an irregular echo pattern. The cumulative incidence of thyroid dysfunction was significantly higher in those with an irregular vs. a regular echo pattern (13/23 [56.5%] vs. 1/19 [5.3%], p = 0.001). None of the patients developed thyroid dysfunction after the initial 24-week period. CONCLUSIONS: The risk of thyroid dysfunction induced by anti-PD-1 antibodies can be predicted by evaluation of anti-thyroid antibodies and the thyroid echo pattern at baseline. TRIAL REGISTRATION: UMIN000019024.

DOI： 10.1038/s41416-020-0736-7

Web of Science

PubMed

Other Link： http://www.nature.com/articles/s41416-020-0736-7

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Papers - ARIMA, Hiroshi