Nicotine, the major addictive substance in cigarette smoke, contributes to smokers' higher risk of developing atherosclerosis, the primary cause of heart attacks, according to research to be presented Sunday, Dec. 15, at the American Society for Cell Biology Annual Meeting in New Orleans.
These findings suggest that e-cigarettes, the battery-powered devices that deliver nicotine in steam without the carcinogenic agents of tobacco smoke, may not significantly reduce smokers' risk for heart disease, said Chi-Ming Hai, Ph.D., of Brown University.
E-cigarettes have put nicotine back in the news and into the hands of a growing number of U.S. smokers who now "vape," that is, inhale a steam of nicotine, polyethylene glucose (PEG) and flavoring generated by cigarette-shaped vaporizers.
Alhough e-cigarettes are being promoted as "safe" nicotine delivery systems, the safety of nicotine has been disputed, partly because the mechanism by which it acts on the circulatory system has not been well understood.
Dr. Hai's research on human and rat vascular smooth muscle cells provides evidence of a link between nicotine and atherosclerosis.
In Dr. Hai's experiments, nicotine appeared to drive the formation of a kind of cellular drill called podosome rosettes, which are members of the invadosome family, consisting of invadopodia, podosomes and podosome rosettes. These specialized cell surface assemblies degrade and penetrate the tissue during cell invasion. Invasion of vascular smooth muscle cells from the middle layer of the arterial wall (media) to the inner layer of the arterial wall (intima) contributes substantially to plaque formation in atherosclerosis.
Dr. Hai subjected rat and primary human vascular smooth muscle cells to prolonged (six hours) nicotine treatment, enabling the cells to form podosome rosettes in response to Protein Kinase C (PKC) activation, which controls protein phosphorylation in signal transducti
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