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首页> 外文期刊>Cellular Physiology and Biochemistry >Downregulation of quinone reductase 2 attenuates vascular smooth muscle cells proliferation and neointimal formation in balloon injured rat carotid artery
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Downregulation of quinone reductase 2 attenuates vascular smooth muscle cells proliferation and neointimal formation in balloon injured rat carotid artery

机译：醌还原酶2的下调减弱了球囊损伤大鼠颈动脉的血管平滑肌细胞增殖和新内膜形成

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摘要

Quinone reductase 2 (NQO2) is a flavoprotein that catalyzes the metabolic reduction of quinines, but its biological mechanism in vascular smooth muscle cells (VSMCs) is unclear. The aim of this study was to evaluate the role of NQO2 on VSMCs proliferation and the neointimal formation in balloon injured rat carotid artery. Methods: Left common carotid arteries from Sprague-Dawley rats were injured by a balloon catheter, and the injured arteries were incubated with 50 μL solution of NQO2-siRNA-GFP lentiviral vectors, NC-siRNA-GFP lentiviral vectors or PBS for 1 h. The rats were euthanized for morphometric and immunohistochemical analysis, real-time PCR and western blot analysis at 2 weeks after balloon injury and gene transfer. The cultured rat VSMCs transduced with NQO2-siRNA-GFP or NC-siRNA-GFP lentiviral vectors were used for cell proliferation assay, real-time PCR and western blot analysis. In order to detect the vascular or intracellular ROS level, the lentiviral vectors without GFP were used to transfect the injured common carotid arteries and the cultured rat VSMCs. Results: Lentiviral vectors bearing NQO2 siRNA could reduce NQO2 protein level and suppress NQO2 mRNA expression in balloon injured artery walls and cultured rat VSMCs. Downregulation of NQO2 significantly suppressed VSMCs proliferation and intimal formation. NQO2 siRNA treatment could reduce vascular or intracellular ROS level and decrease the phosphorylation of the ERK1/2 in balloon injured artery walls and cultured rat VSMCs. Conclusion: Our study suggests that downregulation of NQO2 significantly suppresses VSMCs proliferation and progression of neointimal formation after vascular injury.
机译：醌还原酶2（NQO2）是一种黄酮蛋白，可催化奎宁的代谢减少，但其在血管平滑肌细胞（VSMC）中的生物学机制尚不清楚。这项研究的目的是评估NQO2对球囊损伤大鼠颈动脉中VSMCs增殖和新内膜形成的作用。方法：用球囊导管损伤Sprague-Dawley大鼠的左颈总动脉，并将损伤的动脉与50μLNQO2-siRNA-GFP慢病毒载体，NC-siRNA-GFP慢病毒载体或PBS溶液孵育1小时。在球囊损伤和基因转移后2周，对大鼠进行安乐死以进行形态分析和免疫组化分析，实时PCR和Western印迹分析。用NQO2-siRNA-GFP或NC-siRNA-GFP慢病毒载体转导的培养的大鼠VSMC用于细胞增殖测定，实时PCR和蛋白质印迹分析。为了检测血管或细胞内ROS水平，使用没有GFP的慢病毒载体转染受损的颈总动脉和培养的大鼠VSMC。结果：携带NQO2 siRNA的慢病毒载体可以降低球囊损伤的动脉壁和培养的大鼠VSMC中的NQO2蛋白水平，并抑制NQO2 mRNA表达。 NQO2的下调显着抑制了VSMC的增殖和内膜形成。 NQO2 siRNA处理可以降低血管或细胞内ROS水平，并减少球囊损伤的动脉壁和培养的大鼠VSMC中ERK1 / 2的磷酸化。结论：我们的研究表明，NQO2的下调显着抑制了血管损伤后VSMC的增殖和新内膜形成的进展。

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