| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Research Abstract |
Role of BMPR2 mutation in the pathogenesis of pulmonary arterial hypertension (PAH) has not been established. The inflammatory mechanisms are shown to be involved in clinical and experimental pathology of PAH. This study was planned to clarify the association of inflammatory mechanisms and BMPR2 gene mutation in the context of pulmonary hypertension by using the genetically modified animal models. We administered TNF alpha to BMPR2 hetero knockout (+/-) mice or control mice and assessed pulmonary hypertension and vascular lesions. Twoweek administration of TNF alpha did not induce pulmonary hypertension nor pulmonary vascular disease in the BMPR2 (+/-) mice. GMCSF administration aggravated hypoxia induced pulmonary hypertension in wild type mice, and anti GMCSF antibody administration improved the hypoxia induced pulmonary hypertension. Thus, an association of inflammatory mechanisms induced by reduced BMPR2 with pulmonary hypertension was demonstrated using animal models.
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