molecular signaling mechanism via IP3 receptors in vascular endothelial cells in a state of pulmonary hypertension
Project/Area Number |
22791000
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Pediatrics
|
Research Institution | Keio University |
Principal Investigator |
KODO Kazuki 慶應義塾大学, 医学部, 助教 (10338105)
|
Project Period (FY) |
2010 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
Keywords | 小児循環器学 / 肺高血圧 / IP3受容体 / 肺血管内皮 / 肺血管平滑筋 / VEGF / エンドセリン / モノクロタリン |
Research Abstract |
We have found that type 2 inositol trisphosphate receptor, one of intracellular calcium release channels, is expressed specifically in the vascular smooth muscle cells of the pulmonary arteries not of the systemic arteries nor of the bronchi in the lung tissue, and that disruption of the gene of type 2 inositol trisphosphate receptor might worsen monocrotaline pyrrole-induced pulmonary hypertension. Our results suggest that type 2 inositol trisphosphate receptor might have a role for controlling pulmonary vascular tone and negatively regulate exacerbation of pulmonary hypertension.
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Report
(3 results)
Research Products
(2 results)