2014 Fiscal Year Final Research Report
Mechanism of hypoxia-induced transformation in endothelial cells
| Project/Area Number |
24590381
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Tottori University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAMAKI Toshiaki 徳島大学, 大学院ヘルスバイオサイエンス研究部, 教授 (80179879)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 血管内皮細胞 / 低酸素応答 / HIF |
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| Outline of Final Research Achievements |
Hypoxia-inducible factors (HIFs) in endothelial cells (ECs) help to maintain ECs and promote vascularization, and HIF-2α is abun- dantly expressed in ECs. However, the mechanisms of action of HIF-2α in ECs are not yet fully understood. The aim of this study was to evaluate the in vivo effects of overexpression of HIF-2α in ECs on skin flap survival. A random pattern skin flap was elevated on the dorsum of transgenic mice (Tg mice) with EC-specific HIF-2α conditional overexpression and wild-type littermate control mice. The HIF-2α mRNA and protein levels were significantly increased in the Tg mice when compared with control mice. Tg mice had significantly increased skin flap survival areas when compared with wild- type mice. Moreover, histological examination revealed an increase in the subcutaneous blood vessel counts in the Tg mice. Specific overexpression of HIF-2α in ECs promoted vascu- larization and enhanced skin flap survival in vivo in a mouse model.
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| Free Research Field |
病態医化学
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