NF-¦ÊB pathway mediates vascular smooth muscle response to nicotine

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• 作者：Zhaoxia Wang^a ; ¹ ; Weidong Wu^b ; ¹ ; Maoping Tang^a ; Ying Zhou^a ; Lianyun Wang^a ; Wangjie Xu^a ; ; Zhongdong Qiao^a ; ^{zdqiao@sjtu.edu.cn}
• 关键词：Nicotine ; NF-¦ÊB signaling pathway ; Vascular smooth muscle cell ; Migration ; Cardiovascular disease
• 刊名：The International Journal of Biochemistry and Cell Biology
• 出版年：2013
• 出版时间：February, 2013
• 年：2013
• 卷：45
• 期：2
• 页码：375-383
• 全文大小：1417 K

文摘

Vascular smooth muscle cells (SMCs) and endothelial cells (ECs) play important roles in nicotine-induced cardiovascular disease. To elucidate the mechanism underlying the abnormal SMC behavioral response to nicotine, we investigated the activation of the NF-¦ÊB signal transduction pathway and cell adhesion molecular (CAM) expression on SMCs. Also we used different cell culture manner of SMC sole and EC-SMC co-culture with a 0.4 or a 3 ¦Ìm membrane pore, to observe whether there is a crosstalk between EC/SMC involved in the process of NF-¦ÊB pathway activation. Nicotine-induced effects were observed in SMCs by both monoculture and co-culture with the 3 ¦Ìm-pore size, including the phosphorylation of IKK and I¦ÊB, the shift of transcription factor NF-¦ÊB, and the enhancement of SMC cytoskeleton protein expression and migration ability, but none were observed by co-culture with the 0.4 ¦Ìm-pore size. All of the actions could be distinctly blocked by ¦Á-bungarotoxin (¦Á7 nicotinic receptor inhibitor) or PDTC (NF-¦ÊB suppressor). Flow cytometry analysis showed that the adhesion molecules ICAM-1 and LFA-1 and VCAM-1 and VLA-4 were better expressed similarly on the surface of SMCs in the monoculture and 3 ¦Ìm-pore size co-culture system vs. the 0.4 ¦Ìm co-culture way. The results imply that nicotine induces SMC cytoskeleton protein up-expression and migration via the NF-¦ÊB signaling pathway and that EC-SMC crosstalk via CAM facilitates its response to nicotine.