Cigarette smoke activates caspase-3 to induce apoptosis of human umbilical venous endothelial cells.

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