Fig. 4.

Role of VEGFR2 activation in EC inflammatory activation caused by chronic CS. A: human pulmonary ECs were transfected with VEGFR2-specific or nonspecific siRNA. siRNA-induced protein knockdown was confirmed by Western blot. B: HPAECs transfected with VEGFR2-specific or nonspecific siRNA were subjected to 18% CS for indicated periods of time. Control cells were left under static conditions. Effect of VEGFR2 knockdown on CS-induced ICAM1 and VCAM1 expression was analyzed in control and stretched cells. siRNA-induced VEGFR2 depletion was confirmed by Western blot. β-Actin was used as a normalization control; n = 3; *P < 0.05 vs. nonspecific RNA (ns-RNA). C: cells were treated with vehicle or 5 μM SU-1498 for 30 min before exposure to CS. ICAM1 expression was analyzed by Western blot with corresponding antibody. β-Actin was used as a normalization control; n = 3; *P < 0.05 vs. 18% CS. D: effect of VEGFR2 knockdown on 18% CS-induced IL-8 production was evaluated by ELISA assay. Data are expressed as means ± SD; n = 4, *P < 0.05 vs. ns-RNA.