| Project/Area Number |
25860063
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pharmacology in pharmacy
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| Research Institution | The University of Tokushima |
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Principal Investigator |
ISHIZAWA Keisuke 徳島大学, ヘルスバイオサイエンス研究部, 教授 (60398013)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 血管リモデリング / 動脈硬化 / 血管平滑筋 / Hypoxia inducible factor / アンジオテンシンII / 酸化ストレス / 血管内皮 / HIF-1α / アンジオテンシンII受容体 / hypoxia-inducible factor / レニン－アンジオテンシン系 |
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| Outline of Final Research Achievements |
Hypoxia-inducible factor-1α (HIF-1α) is a transcription factor which regulates expression levels of a lot of genes implicated in cell proliferation, differentiation, angiogenesis, and so on. Recently, several reports have shown that angiotensin II (Ang II) and cytokines can also induce HIF-1α without hypoxic condition, and thus some reports have suggested that HIF-1α plays crucial roles in chronic inflammation. We have elucidated that Ang II-induced vascular remodeling is suppressed by smooth muscle cell (SMC)-specific HIF-1α deficiency. In our study, we showed that SMC-derived HIF-1α contributes to Ang II-induced vascular smooth muscle cell migration, proliferation and hypertrophy, and vascular fibrosis. We suggested that Ang II-induced SMC-derived HIF-1α expression also contributes to activation of Ang II-AT1 receptor signaling axis. The feedback regulation by HIF-1α may play key roles in Ang II-AT1-induced vascular remodeling.
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