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

Abstract

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.

• Authors: J Wang, D E Wilcken, X L Wang
• Journal: Molecular genetics and metabolism (Mol Genet Metab) Vol. 72 Issue 1 Pg. 82-8 (Jan 2001) ISSN: 1096-7192 [Print] United States
• PMID: 11161833 (Publication Type: Journal Article)
• Copyright: Copyright 2001 Academic Press.

Chemical References

• Tumor Suppressor Protein p53
• CASP3 protein, human
• Caspase 3
• Caspases

Topics

• Apoptosis
• Caspase 3
• Caspases (biosynthesis, metabolism)
• Cells, Cultured
• DNA Fragmentation
• Dose-Response Relationship, Drug
• Endothelium, Vascular (enzymology, metabolism, pathology)
• Enzyme Activation
• Humans
• Microscopy, Fluorescence
• Smoking
• Time Factors
• Tumor Suppressor Protein p53 (biosynthesis)
• Umbilical Veins (enzymology, metabolism, pathology)