| Project/Area Number |
05454692
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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 |
Biomedical engineering/Biological material science
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| Research Institution | University of Tokyo |
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Principal Investigator |
ANDO Joji University of Tokyo, Faculty of Medicine, Dept.of Cardiovascular Biomechanics, Visiting Associate Professor, 医学部(医), 客員助教授 (20159528)
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| Co-Investigator(Kenkyū-buntansha) |
KAMIYA Akira University of Tokyo, Faculty of Medicine, Institute of Medical Electronics, Prof, 医学部(医), 教授 (50014072)
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| Project Period (FY) |
1993 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥6,900,000 (Direct Cost: ¥6,900,000)
Fiscal Year 1995: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1993: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | SHEAR STRESS / ENDOTHELIAL CELL / CALCIUM ION / VCAM-1 / ADHESION MOLECULE / BLOOD FLOW / HEMODYNAMIC FORCE / 流れずり応力 / 一酸化窒素 / 細胞内カルシウム / 共焦点レーザ顕微鏡 / 血管内皮細胞 / ATP / セカンドメッセンジャー |
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| Research Abstract |
The results of our present study consists of two major findings. One is that a signal transduction mechanism by which vascular endothelial cells perceive blood flow and transmit the signal into the interior of the cell via calcium ions has been demonstrated. The other one is that endothelial cells alters their expression of adhesion molecules at both mRNA and surface protein levels in response to changes in blood flow. In regard to the flow sensing mechanism, we observed that cultured bovine endothelial cells showed an elevation in intracellular calcium ion concentration when exposed to shear stress in a flow-loading apparatus. The elevation of calcium consentration was shear-stress dependent in the presence of extracellular ATP,which had nothing to do with membrane potential and stretch-activated ion channels, and the main source for the calcium response was an influx of extracellular calcium ions. These findings indicate that calcium ions may play a role in a signal transduction of blood flow by vascular endothelial cells. As for the cell response to blood flow, we demonstrated that fluid shear stress down-regulates the cell surface expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured mouse endothelial cells. The decrease in VCAM-1 expression was due to a suppression of VCAM-1 mRNA induced by shear stress. Thus, blood flow seems to act as a regulator for adhesion molecule expression in endothelial cells.
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