摘要： Nicotine is the major component in cigarette smoke and has been recognized as a risk factor for various cardiovascular diseases such as atherosclerosis. However, the definite pathogenesis of nicotine-mediated endothelial dysfunction remains unclear because hemodynamic factor in most of prior in vitro studies was excluded. To understand how nicotine affects endothelium in the dynamic environment, human umbilical vein endothelial cells were treated by different laminar shear stresses (LSS; 0, 6, 8, and 12 dynes cm −2 ) with and without 10 −4 M nicotine for 12 h in a parallel plate flow system, following detections of cellular morphology and apoptotic level. Our results showed that cells sheared by 12 dynes cm −2 LSS with nicotine excessively elongated and aligned with the flow direction, and exhibited significant apoptosis as compared to the groups with nicotine or LSS alone. We reasoned that the irregular morphological rearrangement and elevated apoptosis were resulted from the interruption of mechanostasis due to cytoskeletal collapse. Furthermore, all the impaired responses can be rescued by treatment with free radical scavenger ascorbic acid (10 −4 M), indicating oxidative stress was likely mediated with the impairments. In summary, our findings demonstrated an essential role of LSS in nicotine-mediated endothelial injury occurring in the physiological environment. 其他題名： Ann Biomed Eng 出版者： New York: Springer US 出版日期： 2015-09-01 出處： Annals of biomedical engineering, 2015-09, Vol.43 (9), p.2220-2230 版權： Biomedical Engineering Society 2015 識別號： ISSN: 0090-6964 識別號： ISSN: 1573-9686 識別號： EISSN: 1573-9686 識別號： DOI: 10.1007/s10439-014-1244-9 識別號： PMID: 25631203
