Junyi Hua1, Yun Xu1, Yuzhou He1, Xuhong Jiang1, Wu Ye1, Zhimin Pan1. 1. Department of Cardiology, The First Affiliated Hospital, Zhejiang University of Traditional Chinese Medicine Hangzhou 310006, Zhengjiang, China.
Abstract
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.
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 injuryrats. 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 injuryrats 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.
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