CD137–CD137L interaction modulates neointima formation and the phenotype transformation of vascular smooth muscle cells via NFATc1 signaling

被引:0
作者
Wei Zhong
Bo Li
Ping Yang
Rui Chen
Cuiping Wang
Zhongqun Wang
Chen Shao
Wei Yuan
Jinchuan Yan
机构
[1] Affiliated Hospital of Jiangsu University,Department of Cardiology
来源
Molecular and Cellular Biochemistry | 2018年 / 439卷
关键词
Atherosclerosis; VSMC; CD137; NFATc1; Phenotype;
D O I
暂无
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学科分类号
摘要
Vascular smooth muscle cell (VSMC) phenotype transformation is an important event in the formation of vessel neointima during lesion progression. CD137 can accelerate plaque formation, but the underlying mechanisms of this process remain unknown. Thus, we investigated the effect of CD137 signaling on VSMC phenotype transformation and potential mechanism underlying this transformation. Mouse recombinant CD137L and anti-CD137 antibody were used to activate or block the CD137 signaling way, respectively. Real-time PCR, immunofluorescence, and western blot analyses were performed to detect the expression of NFATc1 and phenotype markers such as SM-MHC, α-SMA, and vimentin in vivo or in vitro. Inhibition of NFATc1 expression was established by small interfering RNA (siRNA) and lentivirus in vitro and in vivo, respectively. Plenti-virus vector was constructed to overexpress NFATc1. Transwell assay was used to detect the migration ability of cells. The expression of NFATc1 was significantly upregulated by treating VSMCs with CD137L. The contractile phenotype markers decreased, while the synthesis phenotype marker and cell migration increased after CD137 stimulation. This phenomenon can be blocked by combined use of anti-CD137 antibody or siRNA of NFATc1. Overexpression of NFATc1 caused the VSMC phenotype transformation independently. In conclusion, the CD137–CD137L pathway plays an important role in regulating VSMC phenotype transformation via activation of NFATc1 signaling pathway.
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页码:65 / 74
页数:9
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