2009 Fiscal Year Final Research Report
Genetic disruption of all nitric oxide synthase isoforms causes accelerated renal interstitial fibrosis in mice in vivo
| Project/Area Number |
20790605
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Kidney internal medicine
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
MORISADA Naoya University of Occupational and Environmental Health, Japan, 医学部, 非常勤医師 (00389446)
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| Project Period (FY) |
2008 – 2009
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| Keywords | 一酸化窒素合成酵素 / 腎間質線維化 / 片側尿管結紮 / レニン・アンギオテンシン系 |
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| Research Abstract |
The roles of the nitric oxide synthase (NOS) system in vivo still remain to be fully elucidated. We have recently developed mice in which all three NOS isoforms are completely disrupted. I have studied about the roles of the NOS system in renal lesion formation after UUO in triply NOS disrupted mice. We found that complete deletion of the NOS system caused accelerated renal lesion formation in mice in vivo, and renin-angiotensin system was associated in the mechanism.
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