1996 Fiscal Year Final Research Report Summary
Structural and functional analysis of phenotypic modulation of vascular smooth muscle cell
| Project/Area Number |
07457216
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
内分泌・代謝学
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| Research Institution | Chiba University |
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Principal Investigator |
SAITO Yasushi Chiba University School of Medicine Professor, 医学部, 教授 (50101358)
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| Co-Investigator(Kenkyū-buntansha) |
MORI Seijiro Chiba University School of Medicine Assistant, 医学部, 助手 (50270848)
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| Project Period (FY) |
1995 – 1996
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| Keywords | vascular smooth muscle cell / cell growth / cell migration |
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| Research Abstract |
The purpose of this study is to investigate the mechanisms for the phenotypic modulation of vascular smooth muscle cells, which is implicated in the development of atherosclerosis. The study was initiated by our previous observation that the intimal smooth muscle cells show amplified growth potential as well as migratory activity, and they efficiently incorporate the denatured lipoprotein to become foam cells like macrophages. In the present study, we have found that type IV collagen treatment of endothelial cells suppresses the expression of vascular cell adhesion molecule-1, suggesting that vascular smooth muscle cells can change the phenotype of the endothelial cells by secretion of extracellular matrices and such phenomenon plays some role in the developmental process of atherosclerosis. Next, we found that TGF-beta1 administration enhances intimal thickening of the legions made by ballon catheter injury in rabbits, indicating that TGF-beta produced by various cells in atherosclerotic legions accelerates the progression of atherosclerosis possible by promoting the secretion of extracellular matrices from the vascular smooth muscle cells. Finally, we also found that focal adhesion kinase plays an important role in the intracellular signal transduction for chemotaxis stimulated by platelet-derived growth factor downstream of phosphatidylinositol 3-kinase. The findings will reveal the molecular mechanism of the chemotactic signaling inside the cells in response to various extracellular stimuli.
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