| Project/Area Number |
21790748
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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 | Keio University |
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Principal Investigator |
SATOH Takashi Keio University, 医療衛生学部, 助教 (90407114)
|
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| Co-Investigator(Renkei-kenkyūsha) |
KUWANA Masataka 慶應義塾大学, 医学部, 准教授 (50245479)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 肺動脈性高血圧症 / 低酸素 / 血管内皮細胞 / BMP受容体 / シンバスタチン |
|---|
| Research Abstract |
To examine mechanisms for hypoxia-induced pulmonary arterial hypertension (PAH), we identified for hypoxia-responsive genes unique to human pulmonary artery endothelial cells (HPAEC). Aorta and umbilical vein endothelial cells were used as controls. As a result, BMPR-IA and BMPR-II, a receptor for BMP, were identified as genes and proteins down-regulated in hypoxic HPAEC, but not in other endothelial cells. These findings suggest that hypoxia suppresses BMP signaling via down-regulation of BMP receptor in HPAEC, leading to development of PAH. Interestingly, simvastatin reversed the inhibitory effects of hypoxia and restored BMPR mRNA expression in HPAEC, might prevent PAH.
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