Cigarette smoke activates caspase-3 to induce apoptosis of human umbilicalvenous endothelial cells

We explored an hypothesis that cigarette smoking-induced endothelial injury is mediated by accelerated apoptosis by treating human endothelial cells w ith cigarette smoke extracts (CSE). In cells treated with an increasing dos es of CSE (0.005-0.03 cigarette equivalents/mL), we found a dose-dependent increase in the proportion of endothelial cells stained positive for apopto tic changes (8.3 +/- 0.7 to 50.7 +/- 2.2%, P < 0.01), accompanied by change s in caspase-3 activities and p53 protein levels. We suggest that excessive endothelial apoptosis may contribute to cigarette smoke-induced endothelia l dysfunction and hence atherogenesis. (C) 2001 Academic Press.