| Project/Area Number |
21590335
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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 |
Pathological medical chemistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
TOMITA Shuhei 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 准教授 (00263898)
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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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| Research Collaborator |
NAKAYAMA Taisuke 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 大学院生
IMANISHI Masaki 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 大学院生
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 分子病態学 / 低酸素 / 血管内皮細胞 / 低酸素応答 / 肺高血圧症 / 転写因子 / HIF / 微小環境 / 酸化ストレス / 活性酸素 |
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| Research Abstract |
MCT-induced pulmonary arteries demonstrated binding of pimonidazole, a hypoxia detection agent that binds to regions of hypoxia in the region around vascular walls including lung epithelial cells. Indices of the PAH were significantly alleviated in the Hif-1β+/-mice compared to the control as the following data showed ; the weight ratio of right ventricular to left ventricular with septum was significantly decreased ; the number of pulmonary arteries was significantly increased ; indices of the medial thickness was significantly decreased. The number of musculized pulmonary arteries in MCT-treated Hif-1β+/-mice was significantly decreased compared to that of the control mice. In addition, interestingly, the PAH in wild type mice was ameliorated by administration of bosentan, an endothelin receptor blocker, to the same level of that in Hif-1β+/-mice. These results indicate that the development of MCT-induced PAH was mediated by HIF-1βin endothelial cells.
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