Novel therapeutic strategy with Vasohibin against acute kiney injury
| Project/Area Number |
15K09263
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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 |
Kidney internal medicine
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| Research Institution | Okayama University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
SATO Yasufumi 東北大学, 加齢医学研究所, 教授 (50178779)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 急性腎障害 / 血管新生 / ミトコンドリア / 酸化ストレス / アポトーシス / Vasohibin |
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| Outline of Final Research Achievements |
In this study, antiangiogenic factor Vasohibin-1 (VASH1) heterozygous deficiency exacerbated cisplatin-induced acute kidney injury (AKI) with markedly decreased expression of mitochondrial antioxidative enzyme SOD2. Recombinant VASH1 increased SOD2 expression in cultured renal tubular cells. On the other hand, proangiogenic factor Vasohibin-2 (VASH2) homozygous deficiency again exacerbated ischemic-reperfusion AKI. Overexpression of VASH2 in cultured real tubular cells resulted in the inhibition of H2O2-induced apoptosis. Taken together, increased expression of VASH1 and VASH2 in renal tubular cells may be a novel therapeutic strategy against AKI.
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Report
(4 results)
Research Products
(11 results)
