| Project/Area Number |
24790759
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Okayama University |
|---|
Principal Investigator |
TAKEDA Masaya 岡山大学, 医学部, 客員研究員 (80534685)
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 原発性肺高血圧症 / 二次性肺高血圧症 / 骨形成蛋白 / PPARγ |
|---|
| Research Abstract |
The pathogenesis of primary arterial hypertension (PAH) was investigated by focusing on bone morphogenetic protein (BMP) and PPARs in pulmonary artery smooth muscle cells (PASMC). The expression of PPAR-gamma was decreased in PASMC from secondary pulmonary hypertension (SPH) compared with that from PAH. PAH cell proliferation induced by PDGF, ET-1 and BMP was suppressed by PPAR-gamma activation. The reduction of PPAR-gamma expression was related to proliferation of PASMC in response to various vasoactive agents. The expression of BMP receptors was suppressed by the activation of PPAR-gamma in both PAH- and SPH-PASMCs, suggesting the existence of a feedback system of BMP-PPAR in PASMCs. Thus, PPAR-gamma in PASMCs is likely to be involved in the suppression of PASMC proliferation in different ways between PAH and SPH.
|
