| Project/Area Number |
26450414
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Veterinary medical science
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| Research Institution | Nippon Veterinary and Life Science University |
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Principal Investigator |
SUZUKI HIROETSU 日本獣医生命科学大学, 獣医学部, 教授 (50277662)
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| Co-Investigator(Renkei-kenkyūsha) |
YASUDA Hidenori 新潟大学, 医歯学系, 助教 (00806490)
TOCHIGI Yuki 日本獣医生命科学大学, 獣医学部, 講師 (40571576)
KATAYAMA Kentro 日本獣医生命科学大学, 獣医学部, 准教授 (50508869)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 腎臓 / 発生 / 線維化 / ネフロン / mTOR / Astrin / astrin / apoptosis / chonic kidney disease / nephron / mesenchymal cell / kidney / 慢性腎臓病 / 器官発生 |
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| Outline of Final Research Achievements |
Microtubule-associated protein, Astrin, is required for normal progression of mitosis. In interphase, Astrin also regulates mTORC1 pathway by binding to Raptor, which is essential for the activation of mTORC1. In the present study, we examined the role of Astrin in normal renal development and renal pathogenesis using Astrin-deficient rats.
Astrin is expressed in nephron-progenitor-mesenchymal (MM) cells. Astrin-deficient MM cells showed abnormal stemness and increased apoptosis, that is accompanied by the activation of mTORC1. Furthermore, renal fibrosis progressed with age in Astrin-deficient rats was apparently attenuated by mTORC1 inhibitor. A series of experiments demonstrate the function of Astrin and mTORC1 in renal development and renal pathogenesis.
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