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.
Wang
J
J
Cardiovascular Genetics Laboratory, University of New South Wales, Prince Henry and Prince of Wales Hospital, High Street, Randwick, NSW 2031, Australia. xwang@darwin.sfbr.org
Wilcken
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Wang
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D017209:Apoptosis; D053148:Caspase 3; D020169:Caspases / Q000096:biosynthesis / Q000378:metabolism*; D002478:Cells, Cultured; D053938:DNA Fragmentation; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology; D004789:Enzyme Activation; D006801:Humans; D008856:Microscopy, Fluorescence; D012907:Smoking; D013997:Time Factors; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis; D014471:Umbilical Veins / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology
D016159:Tumor Suppressor Protein p53; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases