Cigarette smoking is a risk factor for development of cardiovascular (CV) disease , with increased platelet activation due to cigarette smoke involving a major part of this risk. We have shown that this smoke-induced platelet activation is largely due to the non-nicotine smoke components and their effects can be effectively modulated in the presence of nicotine. However, the effects of nicotine and non-nicotine cigarette smoke components need to be confirmed more physiologically in the presence of endothelial cells (ECs). Prior in-vitro studies have shown that high concentrations of cigarette smoke extract (CSE) increase adhesion molecule expression on ECs. These studies however preclude the involvement of physiological shear stresses and are performed on ECs alone. To overcome these limitations and investigate ECs-platelets together in one system under shear stress, we use a hemodynamic shear device (HSD) that combines features of the cone and plate, and the annular Couette viscometer (to facilitate platelet sampling). We test the following hypotheses — (1) smoke-activated platelets and the nicotine-free extract would confer a synergistic E-selectin expression on ECs, and (2) in contrast to conventional cigarette extracts, nicotine-free smoke extracts would increase platelet activation more significantly, and that this effect may be independent of the presence of ECs.
- Bioengineering Division
E-Selectin Expression on Endothelial Cells in the Presence of Platelets and Cigarette Smoke Extract
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Girdhar, G, Xu, S, Jesty, J, & Bluestein, D. "E-Selectin Expression on Endothelial Cells in the Presence of Platelets and Cigarette Smoke Extract." Proceedings of the ASME 2008 Summer Bioengineering Conference. ASME 2008 Summer Bioengineering Conference, Parts A and B. Marco Island, Florida, USA. June 25–29, 2008. pp. 871-872. ASME. https://doi.org/10.1115/SBC2008-192154
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