Figure 6From: Molecular regulation of the expression of leptin by hypoxia in human coronary artery smooth muscle cells AngII, ROS, and the JNK pathway are involved in leptin expression in HCASMCs under hypoxia. (A and B) Under hypoxia, AngII (10 nM), an ROS generator (Dp44mT; 30 nM)), and a JNK MAPK stimulator (Anisomycin; 20 μM) increased leptin protein expression in HCASMCs. AngII-induced leptin protein expression could be inhibited by SP600125 (25 μM) and NAC (500 μM). Dp44mT-induced leptin protein expression could be inhibited by SP600125 (25 μM). However, Anisomycin-induced leptin protein expression could not be inhibited by losartan (ARB; 100 nM) or NAC (500 μM). These results imply that hypoxia-induced leptin expression in HCASMCs is regulated through the JNK pathway, with its earliest expression coming from treatment with AngII, and then from ROS. *P < 0.01 vs. normoxia control. #P < 0.01 vs. 4 h (n = 3).Back to article page