Laminar Shear Stress Promotes Nicotine-Induced Inflammation and Hemostatic Expression in Human Endothelial Cells

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Title:	Laminar Shear Stress Promotes Nicotine-Induced Inflammation and Hemostatic Expression in Human Endothelial Cells
Authors:	李宇翔;Lee, Yu-Hsiang;Lee, Chi-Chung;Huang, Chien-Hsun;Ho, Feng-Ming
Contributors:	生醫理工學院生醫科學與工程學系
Keywords:	Biological and Medical Physics;Biomaterials;Biomedical Engineering and Bioengineering;Biomedical Engineering/Biotechnology;Biophysics;Cell Biology;Cells;Endothelial cells;Endothelium;Engineering;Gene expression;Hemodynamics;Hemostatics;In vivo methods and tests;Inflammatory diseases;Laminar;Laminates;Nicotine;Nitric oxide;Recombinant;Shear stress;Thromboembolism
Date:	2016-09-01
Issue Date:	2026-04-23 11:16:44 (UTC+8)
Publisher:	Springer New York;New York: Springer US
Abstract:	摘要： Nicotine has been known to play a pathogenic role in various cardiovascular disorders. However, the definite mechanism of nicotine-mediated endothelial dysfunction in vivo remains unclear because hemodynamic factor in most of in vitro studies was excluded. In this study, we investigated how nicotine affects human umbilical vein endothelial cells (HUVECs), from views of inflammatory and hemostatic responses of the cells, under a hemodynamic environment as occurred in vivo . Our results showed that both inflammation, reflected by production of reactive oxygen species and efficacy of monocytes adhesion, and hemostatic expression of HUVECs were abnormally enhanced after treated with 10 −4 M nicotine and 12 dynes cm −2 laminar shear stress (LSS) simultaneously for 24 h, and that the protein expression levels of VCAM-1, ICAM-1, and PAI-1 were significantly enhanced 1.3-, 2- and 2-fold ( p < 0.05 for each), respectively, as compared to the group with nicotine alone; 2.2-, 3- and 4.2-fold ( p < 0.05 for each), respectively, as compared to the group with LSS alone. We reasoned that those irregular expressions were resulted from the reduction of endothelial nitric oxide synthase that was initially caused by nicotine exposure and exacerbated due to LSS treatment. Furthermore, all the impaired responses can be alleviated by use of 1 μ g mL −1 recombinant tissue plasminogen activator, implicating that the irregular inflammation may be due to thrombosis. 其他題名： Cel. Mol. Bioeng 出版者： New York: Springer US 出版日期： 2016-09 出處： Cellular and molecular bioengineering, 2016-09, Vol.9 (3), p.466-477 版權： Biomedical Engineering Society 2016 識別號： ISSN: 1865-5025 識別號： EISSN: 1865-5033 識別號： DOI: 10.1007/s12195-016-0434-y
Appears in Collections:	[Department of Biomedical Sciences and Engineering ] journal & Dissertation

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