| Project/Area Number |
22790700
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| Research Category |
Grant-in-Aid for Young Scientists (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 | Mie University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 血管内皮細胞 / 活性化プロテインC / トロンボモジュリン / ギャップ結合 / コネキシン / 炎症 / 血液凝固 / 血管新生 / 血管病変 / 内皮細胞 |
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| Research Abstract |
Cardiovascular diseases, such as atherosclerosis and thromboembolism, are caused by endothelial dysfunctions associated with pathogenic activation of blood coagulation and inflammation. Our goal is to understand the mechanisms for protection and maintenance of endothelial functions. I first investigated the effects of activated protein C and thrombomodulin on endothelial gap junction. My results demonstrated that these factors enhance gap junction intercellular communication. Next, I indicated that inhibition of gap junction protein connexin32 increases tissue factor expression and that overexpression connexin32 enhances tube formation of endothelial cells. In addition, endothelial cells modulate monocyte/neutrophil activation via gap junction mediated cell-cell interaction. These results suggested activated protein C and thrombomodulin regulate gap junction cell-cell interaction in order to maintain endothelial functions and homeostasis.
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