会议专题

Wnt4/β-catenin signaling pathway modulates balloon-injured carotid artery restenosis via disheveled-1

  Background: Restenosis is a common adverse event of endovascular procedures and troubles cardiologists.However, the mechanism underlying restenosis is still not fully understood.To evaluate whether disheveled-1 (Dvl-1) is involved in the Wnt4/β-catenin signaling pathway to participate in the mechanisms of vascular restenosis.Methodology: Rat model of balloon-injured carotid artery was established and atorvastatin was used to treat artery injury.Vascular smooth muscle cells (VSMC) were isolated from rats and cultured in DMEM exposed to Angll.Downregulation and overexpression of Dvl-1 were conducted in cells to explore the role underlying its effects on VSMC proliferation and collagen expression.Adenovirus with overexpressing Dvl-1 was injected into rats to evaluate the role of Dvl-1 in artery injury rats.Results: The results in vivo found that Wnt4, Dvl-1 and β-catenin expression as well as collagen volume fraction (CVF) in injured artery were significantly increased.The results in vitro showed that Dvl1 overexpression reversed the treatment effects of atorvastatin on VSMCs proliferation and collagen expression.It was also canceled by overexpressing Dvl-1 that the decrease of β-catenin protein treated with atorvastatin in cells exposed to Angll.In addition, treated artery injury rats with atorvastatin, the group with injection of Ad-Dvl-1 had higher levels of intima thickness, intimal/medial area ratio and CVF.Conclusion: Dvl-1 was probably a key regulator in the pathway of wnt4/β-catenin to take part in the vascular restenosis partly, and Dvl-1 is a potential gene to anti-restenosis.

Restenosis wnt disheveled-1 β-catenin statin vascular smooth muscle cells rat

Junyi Hua Yun Xu Yuzhou He Xuhong Jiang Wu Ye Zhimin Pan

Department of Cardiology, The First Affiliated Hospital, Zhejiang University of Traditional Chinese Medicine, Hangzhou 310006, Zhengjiang, China

国内会议

浙江省中西医结合心血管病专业委员会第十六次学术年会

杭州

英文

358-368

2016-05-13(万方平台首次上网日期,不代表论文的发表时间)