| Project/Area Number |
26461606
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Pediatrics
|
|---|
| Research Institution | Mie University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
丸山 一男 三重大学, 医学系研究科, 教授 (20181828)
三谷 義英 三重大学, 医学部附属病院, 准教授 (60273380)
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 肺高血圧 / 炎症 / サイトカイン / 炎症機序 |
|---|
| Outline of Final Research Achievements |
Although the role of BMPR2 mutation in the pathogenesis of pulmonary arterial hypertension (PAH) was not established, association of BMPR2 mutation and inflammatory mechanisms are shown in clinical and experimental pathology of PAH. We have shown that anti GM-CSF antibody administration improved the hypoxia induced pulmonary hypertension. To further elucidate the role of inflammation in PAH, we investigated the role of inflammation in a new human PAH-like rat model induced by the vascular endothelial growth factor receptor blockade with Sugen 5416 in combination with chronic hypoxia. Compared with in controls, the number of perivascular macrophages progressively increased during the experimental period; gene expression of IL6, MCP1, MMP9, cathepsin-S, and RANTES was distinctively upregulated in lungs.
|
