H2型松弛素促进人血管平滑肌细胞迁移的作用及机制  

Role of Relaxin-2 in the migration of human vascular smooth muscle cells and its underlying mechanisms

作　　者：马晓娟[1] 王侠[1] 丁肖华[1] 付毓平 

机构地区：[1]新乡医学院三全学院检验与影像学院,河南新乡453003

出　　处：《重庆医学》2016年第30期4207-4210,4213,共5页Chongqing medicine

摘　　要：目的探讨H2型松弛素(Relaxin-2)对血管平滑肌细胞(VSMCs)迁移的作用及分子机制。方法采用划痕实验和Transwell实验检测Relaxin-2对VSMCs的迁移作用;采用蛋白质印迹法检测其对细胞信号蛋白丝氨酸苏氨酸蛋白激酶(Akt)、细胞外信号调节激酶(ERK)、核因子-κB(NF-κB)p65的影响。结果 Relaxin-2可剂量依赖性促进VSMCs的迁移,应用NF-κB抑制剂BAY 11-7082可阻断Relaxin-2诱导的基质金属蛋白酶-9(MMP-9)和基质金属蛋白酶-2(MMP-2)的表达,磷脂酰肌醇3激酶(PI3K)抑制剂LY294002和ERK抑制剂U0126预处理可以降低Relaxin-2引起的NF-κB p65的激活。结论 Relaxin-2可能通过活化PI3K/Akt和ERK信号通路激活NF-κB p65,进而促进MMP-9和MMP-2的表达,从而诱导VSMCs迁移效应。Objective To investigate the effect and the associated mechanism of Relaxin-2in the migration of human vascular smooth muscle cells（VSMCs）.Methods The migration of VSMCs in responsing to Relaxin-2was evaluated by using wound healing assay and transwell assay,and the cell signaling proteins,including Akt,ERK and NF-κB p65,in responsing to Relaxin-2were measured by using Western blotting assay.Results Relaxin-2can promote the migration of VSMCs in a dose-dependent manner,NF-κB inhibitor BAY11-7082 can block the expression of MMP-9and MMP-2induced by Relaxin-2,pretreatment with PI3 Kinhibitor LY294002and ERK inhibitor U0126 can reduce the activation of NF-κB p65 induced by Relaxin-2.Conclusion NF-κB p65 could be activated by the activation of PI3K/Akt and ERK signaling pathway induced by Relaxin-2,thereby promoting the expression of MMP-9and MMP-2,and inducing VSMCs migration effect.

关 键 词：H2型松弛素 血管平滑肌细胞 迁移 

分 类 号：R54[医药卫生—心血管疾病]