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

International Journal of Clinical and Experimental Pathology

Wu Ye¹  Xuhong Jiang¹  Junyi Hua¹  Zhimin Pan¹  Yun Xu¹  Yuzhou He¹ 

关键词: Restenosis;    wnt;    disheveled-1;    β-catenin;    statin;    vascular smooth muscle cells;    rat;   

DOI  :  

学科分类：生理学与病理学

来源: e-Century Publishing Corporation

【 摘 要 】

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 AngII. Down-regulation 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 Dvl-1 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 AngII. 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.

【 授权许可】

Unknown