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. 2014 Aug 8;15(8):13738–13754. doi: 10.3390/ijms150813738

Figure 2.

Figure 2

(A) Effect of BMP4 on the pulmonary artery smooth muscle cells (PASMCs) survival. Cells were growth-arrested for 24 h and then treated with BMP4 (1–100 ng/mL) subjected to serum withdrawal; (B) BMP4 induced activation of AKT in PASMCs. BMP4 up-regulated the expression of phospho-AKT in a concentration-dependent manner; (C) BMP4 promoted the survival of PASMCs in AKT-dependent manner. PASMCs were treated as the anticipated groups for 24 h and cell viability was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. LY294002 and wortmannin inhibited the protective effect of BMP4 on cell viability in serum deprived conditions; (D) Caspase-3 inhibitor Z-VAD–FMK was examined and the caspase-3 pathway contribution to the serum deprivation (SD)-induced apoptosis process was studied using the MTT assay; (E) Caspase-3 activity was measured by cleavage of the Ac-DEVD–pNA substrate to pNA. All values are denoted as means ± SEM from three or more independent batches of cells. “SD” means serum deprivation; “LY” means LY294002; “W” means wortmannin. * p < 0.05; ** p < 0.01.