| Project/Area Number |
05454280
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Tokyo Metropolitan Institute of Gerontology |
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Principal Investigator |
UEDA Seigo TMIG,Cell Biology, Research Scientist, 細胞生物, 研究員 (00160169)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUSHITA Satoru TMIG,Research Scientist, 酵素生化学, 研究員
大坪 浩一郎 東京都老人総合研究所, 臨床病理学部門, 部長 (20012718)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥4,700,000 (Direct Cost: ¥4,700,000)
Fiscal Year 1994: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1993: ¥3,100,000 (Direct Cost: ¥3,100,000)
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| Keywords | endothelial cells / Cl^- channel / protein kinase A / protein kinase C / Ca^<2+> / shape changes / adenosine Al / プロテインキナーゼC / Clチャンネル / Caチャンネル / 接着分子 / 透過性 |
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| Research Abstract |
We have recently reported that cAMP-induced rapid shrinkage of bovine pulmonary artery endothelial cells are completely prevented by 2.5 mM N-phenylanthranilic acid (NPA), a Cl^- channel blocker (Ueda S.et al., Circ.Res. (1990) 66 : 957-967). In the present study, we report that protein kinase C (PKC) inhibitors induce shape changes in endothelial cells as well as cAMP.Fluorescence-image analysis with 6-methoxy-N- (3-sulfopropyl) quinolium monohydrate (SPQ) showed that PKC inhibitors induce Ca^<2+>-independent Cl^- efflux in endothelial cells. (Ueda S.Jpn.Circ.J.1993). N6-cyclopentyladenosine (CPA), a selective Al agonist, at 10^<-8>M to 10^<-5>M,induced a transent Ca^<2+>-independent Cl^- efflux. This Cl^- efflux was completely inhibited by 10^<-8>M FK453 (a selective Al antagonist), 500ng/ml pertussis toxin, and 2.5mM NPA (Arima M., Ueda S.et al.Biochem.Biophys.Res.Commun.1994). The present study suggests an important role for a Cl^- channel, mediated via PKA,PKC and adenosine Al, in vascular function and in the development of vascular injury and atherosclerosis.
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