Regulation of endothelial cell functions by anticoagulant factors and gap junction.
| 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 |
|---|
| 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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Report
(3 results)
Research Products
(27 results)
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[Journal Article] Connexin32 protects against vascular inflammation by modulating inflammatory cytokine expression by endothelial cells2011
Author(s)
Okamoto, T., Akiyama, M., Takeda, M., Akita, N., Yoshida, K., Hayashi, T., Suzuki, K.
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Journal Title
Experimental Cell Research
Volume: 317
Pages: 348-355
Related Report
Peer Reviewed
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[Journal Article] Activated protein C stimulates osteoblast proliferation via endothelial protein C receptor2010
Author(s)
Kurata, T., Hayashi, T., Yoshikawa, T., Okamoto, T., Yoshida, K., Iino, T., Uchida, A. and Suzuki, K.
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Journal Title
Thrombosis research
Volume: 125
Pages: 184-191
Related Report
Peer Reviewed
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[Journal Article] トロンビン受容体2010
Author(s)
岡本貴行、鈴木宏治
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Journal Title
International Review of Thrombosis(メディカルレビュー社)
Volume: 5
Pages: 200-203
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[Presentation] The inhibition of lung metastasis by inactivation of coagulation activity may lead to dissemination of tumor cells2011
Author(s)
Kunihiro Asanuma, Nobuyuki Akita, Takayuki Okamoto, Tatsuya Hayashi, Tomoaki Yoshikawa, Kakunoshin Yoshida, Yumiko Asanuma, Akihiko Matsumine, Atsumasa Uchida, Akihiro Sudo, Koji Suzuki
Organizer
XXIII Congress of the International Society on Thrombosis and Haemostasis
Place of Presentation
京都国際会議場
Related Report
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