| Project/Area Number |
62570393
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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 |
Circulatory organs internal medicine
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| Research Institution | Osaka University Medical School |
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Principal Investigator |
ONISHI Toshio Osaka University Medical School, Asociate Professor, 医学部, 助教授 (50107041)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUO Keisuke Osaka University Medical School Hospital, Research and Clinical Fellow, 医学部附属病院, 医員 (40156758)
MORIMOT Sigeto Osaka University Medical School, Asistant Professor, 医学部, 助手 (20150336)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1988: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Vascular Smooth Muscle Cells / Proliferation / Glycosaminoglycan / Vitamin D / Intracellular Ca^<2+> / Ca^<2+>-ATPase / Low Density Lipoprotein / 血小板由来成長因子 / 動脈硬化 / 血管平滑筋細胞 / プロスタグランディン / 細胞内カルシウム / 活性型ビタミンD / 血小板由来増殖因子 / カルシウム拮抗剤 |
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| Research Abstract |
1. Research on the Pathogenesis of Atherosclerosis: Proliferation of vascular smooth muscle cells (VSMC) and deposition of lipid is important for the pathogenesis of atherosclerosis.
1) Vascular smooth muscle cells from rat aorta contaied a specific receptor for the 1,25-dihydroxyvitamin D_3 and it stimulated the proliferation and suppressed the synthesis of glycosaminoglycan.
2) Platelet derived growth factor (PDGF) increased intracellular Ca^<2+> concentration ([Ca^<2+>] i) in rabbit chondrocytes and stimulated the synthesis of DNA and glycosaminoglycan. Suramin, an antagonist of PDGF, suppressed the increase of [Ca^<2+>] i and the synthesis of DNA.
3) Low density lipoprotein (LDL) increased [Ca^<2+>] i. LDL caused a release of Ca^<2+> from intracellular Ca^<2+> store through production of inositole trisphosphate (iP_3).
4) A specific receptor for PDGF existed in the basolateral membrane of dog kidney and PDGF stimulated Ca^<2+>- ATPase.
2. Reaserch for the effects of various chemical compounds on the intracellular Ca^<2+> signal system.
1) Prostaglandin F2 and angiotensin II (AII), both of which are strong vasoconstrictor, increased [Ca^<2+>] i in VSMC and caused the release of Ca^<2+> from intracellular Ca^<2+> store. Nicorandil, a vasodilator, suppressed the increase of [Ca^<2+>] i induced by prostaglandin F2 and AII.
2) Valinomycin, a potassium ionophore, suppressed the release of CA^<2+> from intracellular Ca^<2+> store induced by AII but did not suppress those induced by ionomycin, a Ca^<2+> ionophore. However valinomycin did not sauppress the production of iP_3 induced by AII.
3) Nitroglycerin and nicorandil, which are nitrates, stimulated the activities of Ca^<2+>-ATPase in the microsmal fraction of porcine coronary artery smooth muscle cells, but Ca^<2+> channel blockers did not.
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