2016 Fiscal Year Final Research Report
Role of inflammatory mechanism in the experimental model of pulmonary arterial hypertension
Project/Area Number |
26461606
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pediatrics
|
Research Institution | Mie University |
Principal Investigator |
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Keywords | 肺高血圧 / 炎症 / サイトカイン |
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.
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Free Research Field |
小児循環器学
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