| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Outline of Final Research Achievements |
Pulmonary arterial hypertension (PAH) is pathophysiologically characterized with medial thickening of smooth muscle cells (SMCs). LR11 is expressed in intimal smooth muscle cells. This study examined the role of LR11 in pulmonary hypertension.The expression LR11, together with HIF-1α was significantly increased under hypoxic conditions compared with normoxia in mouse lung. Serum sLR11 levels were increased under hypoxic condition. The increased right ventricular systolic pressure, right ventricular hypertrophy and medial thickening in wild-type mice were attenuated in KO mice. The expression of LR11 and HIF-1α was increased in cultured SMCs under hypoxic conditions and the knockdown of HIF-1α abolished the hypoxia-induced LR11 induction. Human study showed that serum sLR11 levels were significantly higher in patients with PAH.The sLR11 levels were positively correlated with pulmonary vascular resistance and mean pulmonary arterial pressure.Soluble LR11 may be a novel biomarker.
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