NF-kappa B pathway mediates vascular smooth muscle response to nicotine

作者：Wang, Zhaoxia; Wu, Weidong; Tang, Maoping; Zhou, Ying; Wang, Lianyun; Xu, Wangjie; Qiao, Zhongdong^*

来源：International Journal of Biochemistry & Cell Biology, 2013, 45(2): 375-383.

DOI：10.1016/j.biocel.2012.10.016

• Nicotine
• NF-kappa B signaling pathway
• Vascular smooth muscle cell
• Migration
• Cardiovascular disease

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-kappa B 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 mu m membrane pore, to observe whether there is a crosstalk between EC/SMC involved in the process of NF-kappa B pathway activation. Nicotine-induced effects were observed in SMCs by both monoculture and co-culture with the 3 pm-pore size, including the phosphorylation of IKK and I kappa B, the shift of transcription factor NF-kappa B, and the enhancement of SMC cytoskeleton protein expression and migration ability, but none Were observed by co-culture with the 0.4 mu m-pore size. All of the actions could be distinctly blocked by alpha-bungarotoxin (alpha 7 nicotinic receptor inhibitor) or PDTC (NF-kappa B 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 mu m-pore size coculture system vs. the 0.4 mu m co-culture way. The results imply that nicotine induces SMC cytoskeleton protein up-expression and migration via the NF-kappa B signaling pathway and that EC-SMC crosstalk via CAM facilitates its response to nicotine.

• 出版日期2013-2
• 单位上海交通大学