1995 Fiscal Year Final Research Report Summary
Molecular and cellalan analysis of abnormality of mesangial cell function as a cause of hypertension
| Project/Area Number |
06671130
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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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 Tokyo |
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Principal Investigator |
NAKAO Akihide University of Tokyo, First Department of Medicine associate professor, 医学部(病), 助手 (10159056)
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| Co-Investigator(Kenkyū-buntansha) |
OHARA Mamiko University of Tokyo, First Department of Medicine associate professor, 医学部(病), 助手 (60261963)
OKUDA Toshihiro University of Tokyo, First Department of Medicine associate professor, 医学部(病), 助手
TANIGUCHI Shigeo University of Tokyo, First Department of Medicine associate professor, 医学部(病), 助手 (50188380)
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| Project Period (FY) |
1994 – 1995
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| Keywords | PAF receptor / EP3receptor / RT-PCR / northern blott |
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| Research Abstract |
We planned to clarify the pathophysiological role of lipid autacoids in the kidney in relation with the development of hypertension. For this purpose, first we tried to determine the localization and the quantitation of the PGE2 receptor EP3 which is linked to inhibitory G protein ; Gi, along nephron segments. We used the mutation RT-PCR method which enabled us to quantitate the expression of mRNA in the material as minute as tubules. The result showed that the mRNA for EP3 was expressed in the distal nephron segments. Though EP3 mRNA was not present in proximal segments in adult rats, it was expressed in proximal segments as well in younger rats. In the next step we investigated into the regulation of the expression of PAF receptor mRNA in cultured rat mesangial cell. We elucidated that PAF itself reduced the PAF receptor mRNA expression in as short as 1 hour by PGE2 of which production was mediated Gi linked PAF receptor. PGE2 was strongly suggested to reduce the expression of PAF receptor mRNA through cAMP accumulation.
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