| Project/Area Number |
16K19417
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Cardiovascular medicine
|
|---|
| Research Institution | Kyoto Prefectural University of Medicine |
|---|
Principal Investigator |
Nakanishi Naohiko 京都府立医科大学, 医学(系)研究科(研究院), 助教 (10637911)
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 肺高血圧症 / カベオラ / カベオリン / キャビン / BMPR2 |
|---|
| Outline of Final Research Achievements |
Emerging evidence suggests that caveolin-1 (Cav1) is associated with pulmonary arterial hypertension. Caveolin regulates caveolar formation and functions together with Cavin. Although Cav1 associated with BMPR2, the role of Cav1 in the mechanism of the development of pulmonary hypertension (PH) has not been well-known.
Cav1 knockout mice revealed pulmonary hypertension. Low-dose FK506 that is reported as activator of BMPR2 reversed pulmonary hypertension in Cav1 knockout mice. Cav1 knockdown in pulmonary arterial endothelial cells (PAEC) suppressed the phosphorylation of Smad 1/5/9 that is a downstream of BMPR2 signaling pathway. Low-dose FK506 reversed the inhibition of Smad 1/5/9 phosphorylation in the PAEC, suggesting that Cav1 regulates the Smad signaling via BMPR2. In addition, overexpression of Cav1 decreased BMPR2 expression, which is reversed by Cavin-1. These findings suggest the possibility that Cavin-Caveolin system has a role in the development of PH through BMP signaling.
|
