1999 Fiscal Year Final Research Report Summary
An analysis of collateral formation and vascular smooth muscle cell migration
| Project/Area Number |
09671214
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Teikyo University (1998-1999)
The University of Tokyo (1997) |
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Principal Investigator |
YASUHARA Hiroshi School of Medicine, Teikyo University, Associate Professor, 医学部, 助教授 (50251252)
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| Co-Investigator(Kenkyū-buntansha) |
HOSOI Yutaka School of Medicine, University of Tokyo, Assistant, 医学部, 助手 (40311625)
HATAKEYAMA Takuya School of Medicine, University of Tokyo, Assistant, 医学部, 助手 (60291324)
SHIGEMATSU Hiroshi School of Medicine, University of Tokyo, Associate Professor, 医学部, 助教授 (40134556)
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| Project Period (FY) |
1997 – 1999
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| Keywords | Smooth muscle cell / Endothelial cell / migration / collatenal circulation / Shear stress / platelet / PDGF |
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| Research Abstract |
Migration and proliferation of smooth muscle cells (SMC) are the main mechanisms of development of collateral formation to ischemic organs. However, it has not yet been elucidated how mechanical stress is involved in this process. We investigated smooth muscle cell mitogenic activity induced by shear-loaded platelets and endothelial cells. METHODS: Experimental design: in vitro experimental study. We devised four types of conditioned media; supernatant of mixed culture of platelets and endothelial cell (ST), supernatant of shear-loaded mixed culture of platelets and endothelial cell (SH), ST medium neutralised with anti-PDGF antibody (ST+), and SH medium neutralised with anti-PDGF antibody (SH+). Smooth muscle cells were cultured in each conditioned medium, and their spreading activity was determined under a microscope. RESULTS: Smooth muscle cells spreading activity in the SH group was significantly greater than that in the ST group. Their spreading activity was suppressed by anti-PDGF antibody under shear conditions (SH+), but it was not by anti-PDGF antibody under static conditions (ST+). CONCLUSIONS: Our results demonstrate that platelet-derived growth factor is produced by shear-loaded platelets and endothelial cells, and local mechanical forces may play an important role in cardiovascular disease.
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