Potential role of sustained jnk activation in vascular cell apoptosis

摘要

Our previous studies showed an acceleration of the endothelial cell cycle, e.g., increase in the frequency of cell death leads to the formation of leaky junctions and enhanced macromolecular permeability [1-3]. In this study we examined the molecular basis of programmed death (apoptosis) of vascular endothelial cells and smooth muscle cells by applying two forms of mechanical forces (laminar shear stress and cyclic stretch) and a chemical stimulus (the microtubule-disrupting agent colchicine). The results suggest that a sustained activation of Jun amino-terminal kinase (JNK) may play a significant role in inducing apoptosis.