Journal
MOLECULAR GENETICS AND METABOLISM
Volume 72, Issue 1, Pages 82-88Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/mgme.2000.3115
Keywords
cigarette smoking extracts; endothelial; apoptosis; caspase-3; p53; atherosclerosis
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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. (C) 2001 Academic Press.
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