Updated on 2024/03/21

写真a

 
Ishii Toshihisa
 
Organization
Graduate Faculty of Interdisciplinary Research Faculty of Medicine Clinical Medicine (Nephrology) Clinical Assistant Professor
Title
Clinical Assistant Professor
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Education

  • University of Yamanashi   Integrated Graduate School of Medicine, Engineering, and Agricultural Sciences

    2016.4 - 2020.3

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    Country： Japan

    Course： Doctor course

  • University of Yamanashi   Faculty of Medicine

    2006.4 - 2012.3

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    Country： Japan

Degree

  • Doctor of Philosophy (Medical Science) ( 2020.3   University of Yamanashi )

Research Areas

  • Life Science / Nephrology

  • Life Science / Metabolism and endocrinology

Papers

  • Membrane protease prostasin promotes insulin secretion by regulating the epidermal growth factor receptor pathway Reviewed Major achievement

    Toshihisa Ishii, Yoshikazu Miyasato, Masashi Ichijo, Kohei Uchimura, Fumihiko Furuya

    Scientific Reports   13 ( 1 )   2023.6(  eISSN：2045-2322 )

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

    Abstract

    Prostasin (PRSS8) is a serine protease that metabolizes and moderates the effect of specific substrates. Epidermal growth factor receptor (EGFR), which modulates insulin secretion and pancreatic β-cell proliferation, is regulated via proteolytic shedding by PRSS8. We first detected PRSS8 expression in β-cells of pancreatic islets of mice. To better understand the molecular processes involved in PRSS8-associated insulin secretion, pancreatic β-cell-specific PRSS8 knockout (βKO) and PRSS8-overexpressing (βTG) male mice were generated. We found that glucose intolerance and reduction in glucose-stimulated insulin secretion developed in βKO mice compared with the control subjects. A higher response to glucose was noted in islets retrieved from βTG mice. Erlotinib, a specific blocker of EGFR, blocks EGF- and glucose-stimulated secretion of insulin among MIN6 cells, and glucose improves EGF release from β-cells. After silencing PRSS8 in MIN6 cells, glucose-stimulated insulin secretion decreased, and EGFR signaling was impaired. Conversely, overexpression of PRSS8 in MIN6 cells induced higher concentrations of both basal and glucose-stimulated insulin secretion and increased phospho-EGFR concentrations. Furthermore, short-term exposure to glucose improved the concentration of endogenous PRSS8 in MIN6 cells through inhibition of intracellular degradation. These findings suggest that PRSS8 is involved in glucose-dependent physiological regulation of insulin secretion via the EGF–EGFR signaling pathway in pancreatic β-cells.

    DOI： 10.1038/s41598-023-36326-7

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    Other Link： https://www.nature.com/articles/s41598-023-36326-7

  • 山梨県CKD病診連携と当科における血液透析導入患者の検討

    小西 真樹子, 高橋 和也, 石井 俊史, 高橋 祐子, 内村 幸平, 古屋 文彦

    日本腎臓学会誌   64 ( 3 )   285 - 285   2022.5( ISSN：0385-2385  eISSN：1884-0728 )

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    Language：Japanese   Publisher：(一社)日本腎臓学会  

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  • サクビトリルバルサルタン(ARNI)を安全に導入できた心不全増悪を繰り返す腹膜透析患者の一例

    内村 幸平, 諏訪 博史, 高橋 和也, 小西 真樹子, 石井 俊史, 大越 貴絵, 小佐野 慧一, 諏訪 裕美, 佐藤 泰代

    日本透析医学会雑誌   55 ( Suppl.1 )   772 - 772   2022.5( ISSN：1340-3451  eISSN：1883-082X )

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    Language：Japanese   Publisher：(一社)日本透析医学会  

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  • Intelectin1 ameliorates macrophage activation via inhibiting the nuclear factor kappa B pathway.

    Hidetoshi Kobayashi, Kohei Uchimura, Toshihisa Ishii, Kazuya Takahashi, Kentaro Mori, Kyoichiro Tsuchiya, Fumihiko Furuya

    Endocrine journal   2021.12

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

    Inteletin1 (Itln1) is an adipokine that is abundantly expressed in intestine, ovary, and lung. The expression levels of ITLN1 are decreased in the presence of diabetes or obesity, but the mechanisms of its production and function are still controversial. The aim of this study is to elucidate the mechanisms of ITLN1 synthesis and ITLN1-associated macrophage activation. To analyze the effects of high fat and high-carbohydrate diet (HFHCD) on the expression of ITLN1 in the intestine, the mice were fed a HFHCD for 8 weeks. HFHCD feeding enhanced the endoplasmic reticulum (ER)-stress in the intestine and inhibited the expression of Itln1 in the intestinal endocrine cells and lowered circulating ITLN1 levels. In contrast, treatment with a chemical chaperone and reduction of ER-stress restored the expression of Itln1 in the intestine of HFHCD-fed mice. Furthermore, in vitro studies indicated that ITLN1 physically interacts with adiponectin receptor 1 and suppresses lipopolysaccharide-induced mRNA expressions of pro-inflammatory cytokines and phagocytosis activities via inhibition of the nuclear factor kappa B-signaling pathway in macrophages. These results suggest that diet-induced ER-stress decreases circulating ITLN1 via inhibition of its synthesis in the intestine, and a reduction of circulating ITLN1 might enhanced the expression of proinflammatory cytokines and macrophage activation, following exacerbate the chronic inflammation of metabolic syndrome.

    DOI： 10.1507/endocrj.EJ21-0438

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  • ミコフェノール酸モフェチルが有効だったグルココルチコイド抵抗性特発性膜性腎症の1例

    小西 真樹子, 高橋 和也, 花井 俊一朗, 小佐野 慧一, 諏訪 博史, 石井 俊史, 内村 幸平, 古屋 文彦

    日本腎臓学会誌   63 ( 8 )   1007 - 1013   2021.11( ISSN：0385-2385  eISSN：1884-0728 )

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    Language：Japanese   Publisher：(一社)日本腎臓学会  

    症例は78歳の女性,両下腿の圧痕性浮腫と健康診断で指摘された蛋白尿のため,当科に紹介された。初診時,尿蛋白/クレアチニン比(urine protein/creatinine ratio:UPCR)24.0g/gCr,血清アルブミン1.8g/dLであり,ネフローゼ症候群を呈していた。経皮的腎生検を行ったところ,病理組織で巣状に基底膜のスパイク形成があり,基底膜上皮下にIgG4優位のIgGおよびC3沈着を認めた。電子顕微鏡においても基底膜上皮下沈着物を認め,膜性腎症と診断した。二次性膜性腎症の原因となる所見はなく,血清抗ホスホリパーゼA2受容体(M-Type phospholipase A2 receptor:PLA2R)抗体が陽性だったため,特発性膜性腎症と診断した。プレドニゾロン(prednisolone:PSL)40mg/日とシクロスポリンA(cyclosporine A:CyA)50mg/日内服で初期治療を開始したが,治療反応は不良であり,途中ミゾリビン(mizoribine:MZB)100〜150mg/日内服を追加した。しかし,初期治療から6ヵ月後も寛解を達成できず,蛋白尿が持続した。そのため,CyAとMZBをミコフェノール酸モフェチル(mycophenolate mofetil:MMF)1,500mg/日へ変更したところ,UPCRは徐々に低下し,PSL減量が可能になった。PSL 5mg/日まで減量した時点でも不完全寛解1型を維持できた。MMFは,グルココルチコイド抵抗性特発性膜性腎症に対する追加治療選択肢の一つとなりうる。(著者抄録)

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  • Hyperthyroidism exacerbates ischemic reperfusion injury in the kidney.

    Yasuno Yamaguchi, Kohei Uchimura, Kazuya Takahashi, Toshihisa Ishii, Shunichiro Hanai, Fumihiko Furuya

    Endocrine journal   69 ( 3 )   263 - 272   2021.10

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

    Thyroid hormones are critical regulators of vertebrate development and metabolism. Under hyperthyroid conditions, excess thyroid hormones induce expression of several enzymes and activities via activation of ligand-bound thyroid hormone receptors (TRs). Arginase (ARG) is downstream of a ligand-bound TR and overexpression of ARG2 induces the production of reactive oxygen species and subsequent exacerbation of kidney ischemia/reperfusion (I/R) injury. To clarify the association between I/R-induced kidney injury and hyperthyroidism, mice were pretreated with L-thyroxine (LT4) or vehicle alone, then subjected to I/R. Proximal tubular cell-specific conditional knockout of thyroid hormone receptor β (TRβcKO) mice was generated and the effects of I/R were analyzed. Hyperthyroidism enhanced tubular damage and fibrosis in the kidneys of mice after I/R. Hyperthyroidism induced tubular cell necroptosis following inflammatory cell accumulation in the kidney after I/R. ARG2 expressions and reactive oxygen species accumulated in the kidneys of hyperthyroid mice after I/R, but these changes were ameliorated in the kidneys of TRβcKO mice. Hyperthyroidism-enhanced kidney injury was ameliorated in the kidney of TRβcKO mice after I/R. These results suggest that excess thyroid hormones are disadvantageous for the kidney under ischemic stress. Overt hypothyroidism represents a severe thyroid hormone deficiency disease that requires LT4 treatment, while overreplacement or iatrogenic thyrotoxicosis might cause kidney injury.

    DOI： 10.1507/endocrj.EJ21-0395

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  • Hypoxia-induced thyroid hormone receptor expression regulates cell-cycle progression in renal tubule epithelial cells.

    Shunichiro Hanai, Kohei Uchimura, Kazuya Takahashi, Toshihisa Ishii, Takahiko Mitsui, Fumihiko Furuya

    Endocrine journal   68 ( 11 )   1309 - 1320   2021.6

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

    Hypoxia occurs in the kidneys of chronic kidney disease (CKD) patients, inducing interstitial fibrosis and tubule cell death. Renal tubule cell death is an important determinant of mortality in CKD. We focused on the regulation of cell-cycle-mediated protein expression to prevent cell death under chronic hypoxia in the kidneys of CKD patients. Paraffin-embedded kidney sections from patients with CKD (diabetes nephropathy, nephrosclerosis, or IgA nephropathy) were analyzed for the expression of hypoxia-inducible factor (HIF), thyroid hormone receptor (TR) β, or p21 and levels of interstitial fibrosis. Human renal proximal tubule cells were exposed to hypoxia and analyzed for the expression of HIF, TRβ, or p21 and the cell-cycle stage. TRβ expression was enhanced early on when fibrosis was not fully developed in the tubule cells of CKD patients. HIF1α bound to the TRβ promoter and directly induced its transcription. Further, HIF1α expression induced the expression of TRβ and inhibited cell-cycle progression. In the early stage of kidney injury, TRβ might act as a guardian to prepare and organize cell-cycle proliferation and prevent cell death. While the molecular mechanism that regulates the expression of cell-cycle regulators in renal tubule cells remains controversial, TRβ has strong potential as a new therapeutic target.

    DOI： 10.1507/endocrj.EJ21-0245

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  • 限局皮膚硬化型全身性強皮症に腎クリーゼを合併した1例

    大越 貴絵, 高橋 和也, 朝比奈 謙吾, 石井 俊史, 小佐野 慧一, 小西 真樹子, 諏訪 博史, 内村 幸平, 古屋 文彦

    日本透析医学会雑誌   54 ( Suppl.1 )   348 - 348   2021.5( ISSN：1340-3451  eISSN：1883-082X )

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    Language：Japanese   Publisher：(一社)日本透析医学会  

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  • 術前抗体価著明高値(1024倍)血液型不適合腎移植の一例

    内村 幸平, 高橋 和也, 朝比奈 謙吾, 小佐野 慧一, 諏訪 博史, 石井 俊史, 小西 真樹子, 神家満 学, 古屋 文彦

    日本透析医学会雑誌   54 ( Suppl.1 )   464 - 464   2021.5( ISSN：1340-3451  eISSN：1883-082X )

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    Language：Japanese   Publisher：(一社)日本透析医学会  

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  • プロスタシンは膵β細胞におけるインスリン分泌と細胞増殖を制御する

    石井 俊史, 一條 昌志, 内村 幸平, 古屋 文彦

    糖尿病   64 ( Suppl.1 )   YIA - 2)   2021.5( ISSN：0021-437X  eISSN：1881-588X )

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    Language：Japanese   Publisher：(一社)日本糖尿病学会  

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  • 膵β細胞プロスタシンによるインスリン分泌制御機構の解明

    石井 俊史, 一條 昌志, 内村 幸平, 小林 秀俊, 滝澤 壮一, 古屋 文彦

    糖尿病   63 ( Suppl.1 )   S - 257   2020.8( ISSN：0021-437X  eISSN：1881-588X )

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    Language：Japanese   Publisher：(一社)日本糖尿病学会  

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  • Angiopoietin-Like Protein 2 Promotes the Progression of Diabetic Kidney Disease Reviewed Major achievement

    Toshihisa Ishii, Fumihiko Furuya, Kazuya Takahashi, Miho Shikata, Takeyuki Takamura, Hidetoshi Kobayashi, Asako Miyazaki, Jun Morinaga, Kazutoyo Terada, Yuichi Oike, Eiichiro Kanda, Kenichiro Kitamura

    The Journal of Clinical Endocrinology & Metabolism   104 ( 1 )   172 - 180   2019.1( ISSN：0021-972X  eISSN：1945-7197 )

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：The Endocrine Society  

    DOI： 10.1210/jc.2017-02705

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  • Association between the Cardio-Ankle Vascular Index and Diabetes Mellitus-Related Peripheral Arterial Disease in Chronic Hemodialysis Patients Reviewed

    Fumihiko Furuya, Ai Motosugi, Kazutaka Haraguchi, Shunichiro Hanai, Toshihisa Ishii, Yasuno Yamaguchi, Kenichiro Kitamura

    Blood Purification   47 ( Suppl. 2 )   25 - 30   2019( ISSN：0253-5068  eISSN：1421-9735 )

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：S. Karger AG  

    DOI： 10.1159/000496632

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  • Chronic Inflammation and Progression of Diabetic Kidney Disease Reviewed

    Fumihiko Furuya, Toshihisa Ishii, Kenichiro Kitamura

    CKD-Associated Complications: Progress in the Last Half Century   33 - 39   2019( ISSN：0302-5144  eISSN：1662-2782 )

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    Language：English   Publishing type：Part of collection (book)   Publisher：S. Karger AG  

    DOI： 10.1159/000496526

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  • レパグリニド(RPG)とクロピドグレル(CPG)併用により重症低血糖を来した2例 Reviewed

    石井 俊史, 若杉 正清, 長沼 司, 温井 郁夫, 井口 楓, 井上 正晴, 神宮寺 禎巳

    糖尿病   61 ( 8 )   572 - 572   2018.8( ISSN：0021-437X )

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  • レパグリニドとクロピドグレル併用による遷延性重症低血糖の1例

    石井 俊史, 若杉 正清, 長沼 司, 温井 郁夫, 井口 楓, 井上 正晴, 神宮寺 禎巳

    糖尿病   60 ( 6 )   461 - 465   2017.6( ISSN：0021-437X )

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    Language：Japanese   Publisher：(一社)日本糖尿病学会  

    症例は89歳男性。54歳頃に2型糖尿病と診断され、レパグリニド1.5mg/日、テネリグリプチン20mg/日、ボグリボース0.6mg/日の内服を行っていた。閉塞性動脈硬化症に対しクロピドグレル75mg/日の内服開始翌日の夕食後に低血糖昏睡で入院となった。経口血糖降下薬はすべて中止したが、第3病日まで低血糖が遷延した。退院後、再度併用を開始した2日後の夕食後に再び同様の重症低血糖で入院し、第2病日まで低血糖が遷延した。レパグリニドは短時間作用型のインスリン分泌促進薬であり、単独では遷延性低血糖を来しにくい。Tornioらは、クロピドグレルによるCYP2C8の阻害がレパグリニド血中濃度を上げると報告したが、本症例はこの機序による低血糖と推測された。両薬剤は大血管障害を有する糖尿病患者において併用されることも多く、併用の際には相互作用による低血糖に十分注意する必要がある。(著者抄録)

    DOI： 10.11213/tonyobyo.60.461

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  • The ligand-bound thyroid hormone receptor in macrophages ameliorates kidney injury via inhibition of nuclear factor-kappa B activities Reviewed

    Fumihiko Furuya, Toshihisa Ishii, Shogo Tamura, Kazuya Takahashi, Hidetoshi Kobayashi, Masashi Ichijo, Soichi Takizawa, Masahiro Kaneshige, Katsue Suzuki-Inoue, Kenichiro Kitamura

    SCIENTIFIC REPORTS   7   43960   2017.3( ISSN：2045-2322 )

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    Language：English   Publishing type：Research paper (scientific journal)   Publisher：NATURE PUBLISHING GROUP  

    In chronic kidney disease (CKD) patients, inflammation plays a pivotal role in the progression of renal fibrosis. Hypothyroidism is associated with an increased occurrence of atherosclerosis and inflammation, suggesting protective roles of thyroid hormones and their receptors against inflammatory processes. The contribution of thyroid hormone receptors to macrophage differentiation has not been well documented. Here, we focused on the endogenous thyroid hormone receptor a (TR alpha) in macrophages and examined the role of ligand-bound TRa in macrophage polarization-mediated anti-inflammatory effects. TR alpha-deficient irradiated chimeric mice showed exacerbated tubulointerstitial injury in a unilateral ureteral obstruction model. Compared with wild-type macrophages, macrophages isolated from the obstructed kidneys of mice lacking TRa displayed increased expression of proinflammatory cytokines that was accompanied by enhanced nuclear translocation of p65. Comparison of TRa-deficient bone marrow-derived macrophages with wild-type macrophages confirmed the propensity of the former cells to produce excessive IL-1 beta levels. Co-culture of these macrophages with renal epithelial cells induced more severe damage to the epithelial cells via the IL-1 receptor. Our findings indicate that ligand-bound TRa on macrophages plays a protective role in kidney inflammation through the inhibition of NF-kappa B pathways, possibly by affecting the pro-and anti-inflammatory balance that controls the development of CKD.

    DOI： 10.1038/srep43960

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  • DICREASED SERUMOMENTIN IS ASSOCIATED WITH RISK OF CADIORENAL DYSFUNCTION IN DIABETES PATIENTS

    Toshihisa Ishii, Hidetoshi Kobayashi, Fumihiko Furuya, Kenichiro Kitamura

    NEPHROLOGY DIALYSIS TRANSPLANTATION   30   2015.5( ISSN：0931-0509  eISSN：1460-2385 )

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    Language：English   Publishing type：(MISC) Summary of the papers read (international conference)   Publisher：OXFORD UNIV PRESS  

    DOI： 10.1093/ndt/gfv174.48

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  • 菌血症性ショックを契機に急性腎不全を発症するも透析を離脱しえた1例

    石井 俊史, 古屋 文彦, 内村 幸平, 高橋 和也, 北村 健一郎

    日本透析医学会雑誌   48 ( Suppl.1 )   453 - 453   2015.5( ISSN：1340-3451  eISSN：1883-082X )

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  • 糖尿病患者における血中omentin値と心血管病変発症の関連の検討

    小林 秀俊, 古屋 文彦, 石井 俊史, 高橋 和也, 内村 幸平, 北村 健一郎

    日本腎臓学会誌   57 ( 3 )   582 - 582   2015.4( ISSN：0385-2385  eISSN：1884-0728 )

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Books and Other Publications

  • Liddle 症候群

    （ Role： Contributor）

    診断と治療社  2017.11 

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    Language：Japanese   Book type：Textbook, survey, introduction

Presentations

  • ANGPTL2は糖尿病性腎臓病を進展させる

    石井 俊史, 古屋 文彦, 高橋 和也, 四方 美穂, 高村 武之, 小林 秀俊, 宮崎 朝子, 北村 健一郎

    日本腎臓学会誌  2018.4 

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  • 新規透析導入患者の血管病変発症と血中Angptl2との関連の検討

    小佐野 慧一, 古屋 文彦, 高橋 和也, 石井 俊史, 小西 真樹子, 高村 武之, 秋山 大一郎, 北村 健一郎

    日本腎臓学会誌  2018.4 

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  • CKD精査目的のクリニック受診患者へのDVDを用いた説明

    飯野 美代, 安達 潤子, 小林 京子, 相馬 悦子, 筒井 裕子, 齊藤 慶子, 梅田 恵梨香, 河西 玉江, 小林 秀俊, 石井 俊史, 北村 健一郎, 原口 和貴

    日本腎臓学会誌  2017.4 

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  • 腎障害時の尿細管上皮細胞における甲状腺ホルモンの代謝と抗炎症作用の検討

    石井 俊史, 古屋 文彦, 小林 秀俊, 高橋 和也, 北村 健一郎

    日本腎臓学会誌  2017.4 

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  • 腎障害時に組織マクロファージはAngptl2を産生する

    高村 武之, 四方 美穂, 奥 哲治, 小林 秀俊, 石井 俊史, 渡邊 美教, 高橋 祐子, 高橋 和也, 秋山 大一郎, 古屋 文彦, 北村 健一郎

    日本腎臓学会誌  2017.4 

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  • 腎障害下尿細管上皮細胞における脱ヨウ素酵素の作用の検討

    石井 俊史, 古屋 文彦, 一條 昌志, 滝澤 壮一, 金重 勝博, 北村 健一郎

    日本内分泌学会雑誌  2017.4 

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  • 糖尿病性腎症におけるアルブミン尿の増悪と血中Angptl2値の関連性の検討

    渡邉 美教, 奥 哲治, 四方 美穂, 高村 武之, 小林 秀俊, 石井 俊史, 高橋 祐子, 高橋 和也, 秋山 大一郎, 古屋 文彦, 北村 健一郎

    日本腎臓学会誌  2017.4 

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  • omentin 1はpodocyte調整作用を介し糖尿病性腎症の進展を抑制する

    小林 秀俊, 古屋 文彦, 石井 俊史, 高橋 和也, 北村 健一郎

    日本腎臓学会誌  2017.4 

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Awards

  • Young Investigators Award

    2018   日本病態プロテアーゼ学会   プロスタシンによる膵細胞インスリン分泌の制御

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

  • 奨励賞

    2016   Kidney Summit   腎障害下の尿細管細胞とマクロファージとの甲状腺ホルモンを介したクロストーク

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

Teaching Experience (On-campus)

  • チュートリアルコース3

    2023Year

  • 疾病・治療論Ⅰ

    2023Year  Type of subject：Professional education (undergraduate)

    腎疾患の診断・治療

  • 疾病・治療論Ⅰ

    2022Year  Type of subject：Professional education (undergraduate)

    腎疾患・自己免疫疾患の診断・治療

  • チュートリアルコース3

    2022Year  Type of subject：Professional education (undergraduate)

  • 疾病・治療論Ⅰ

    2021Year  Type of subject：Professional education (undergraduate)

    腎疾患・自己免疫疾患の診断・治療

  • チュートリアルコース3

    2021Year  Type of subject：Professional education (undergraduate)

  • 疾病・治療論Ⅰ

    2020Year  Type of subject：Professional education (undergraduate)

    腎疾患・自己免疫疾患の診断・治療

  • チュートリアルコース3

    2020Year  Type of subject：Professional education (undergraduate)

    Primary and Secondary Glomerulonephritis

▼display all

Other educational achievements

  • 山梨県キャリア形成卒前支援プロジェクト「山梨県生活習慣病未来共創セミナー」

    2023

  • あおぎり講座　担当教員

    2023

  • やまなしジュニアドクター育成塾担当教員

    2023

Social Activities

  • ゼロから始める山梨の健康づくり　PROJECT ZERO

Professional Memberships

  • 日本内科学会

    2014.3

  • 日本糖尿病学会

    2014.11

  • 日本腎臓学会

    2015.1

  • 日本透析医学会

    2015.2

  • 日本腎臓リハビリテーション学会

    2021.9