Synergistic Impact of Nicotine and Shear Stress Induces Cytoskeleton Collapse and Apoptosis in Endothelial Cells

Yu Hsiang Lee, Ruei Siang Chen, Nen Chung Chang, Kueir Rarn Lee, Chien Tsai Huang, Yu Ching Huang, Feng Ming Ho

研究成果: 雜誌貢獻文章同行評審

5 引文 斯高帕斯(Scopus)

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.

原文英語
頁(從 - 到)2220-2230
頁數11
期刊Annals of Biomedical Engineering
43
發行號9
DOIs
出版狀態已發佈 - 9月 29 2015

ASJC Scopus subject areas

  • 生物醫學工程

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