Fig. 3.

Hypoxia-induced bPASMC proliferation is blocked by TG2 inhibitor ERW1041E and TG2 cross-linking defective mutant C277V. A: serum-starved bPASMCs were pretreated with TG2 inhibitor ERW1041E for 1 h and exposed to normoxia (21% O₂) or hypoxia (3% O₂) for 24 h. B: bPASMCs were either mock transfected or transfected with pcDNA vector alone or with TG2 point mutants, the GTP-binding defective R580L, and the cross-linking defective C277V. Control cells were treated with transfection reagent alone. The next day bPASMCs were serum starved and then exposed to normoxia or hypoxia for 24 h. Cell proliferation was quantified by [³H]thymidine incorporation assay and expressed as cell counts (n = 12 wells/treatment group). *P < 0.05, significantly different from vehicle-treated or mock-transfected normoxia control. #P < 0.05, significantly different from vehicle-treated or mock-transfected hypoxia control.