摘要
探讨转化生长因子-β1(Transforming growth factor,TGF-β1)在介入性血管损伤后新生内膜的形成过程中发挥的作用以及TGF-β1对间充质干细胞(MSCs)可能与新生内膜的发生发展存在的关系。本实验通过建立大鼠颈总动脉球囊损伤模型,检测动脉损伤后不同时间点新生内膜中各蛋白的表达变化,以探讨TGF-β1/Smad信号通路的活化与内膜增生以及TGF-β1与MSCs招募的关系。以计算机图像分析系统计算损伤血管内膜增生程度的变化,免疫组化En Vision二步法检测血管损伤后7、14、21 d时新生内膜中TGF-β1、P-Smad2/3、Nestin及Ki-67的蛋白表达。结果显示:(1)大鼠颈动脉球囊损伤后不同时间点血管内膜增生程度不同,损伤后7 d开始形成少量内膜,14d显著增多,21 d达最大厚度;(2)TGF-β1、P-Smad2/3于新生内膜中的表达含量变化与Ki-67阳性指数正相关;(3)Nestin在损伤血管内的表达阳性指数与TGF-β1的表达量正相关。由此可知,TGF-β1对血管损伤后内膜增生的促进作用可能通过Smad经典信号通路,且在损伤过程中,TGF-β1的分泌可能招募循环中的MSCs至损伤血管处,共同参与损伤后的血管重塑。
Mechanisms of Transforming growth factor(TGF)-β1 involving in neointima formation are still controversial.It has been suggested that the recruited mesenchymal stem cells(MSCs) following arterial injury could contribute to neointima formation,but the role of downstream signaling and the contribution of the recruited MSCs are still unknown.In this study,we observed the correlations between expression and distribution of TGF-β1/Smad signaling pathway proteins and recruitment of MSC cells in the process of neointima formation using a rat model for balloon-induced carotid artery injury.It was found that the neointima thickness increased to the maximum at 21 days; Ki-67 expression was increased consistent with the elevation of TGF-β1 and p-Smad2/3 levels; MSCs accumulated at the lumen side of neointima.Herein,It was demonstrate that TGF-β1induced the proliferation of neointima cells by Smad signaling and MSCs recruited by TGF-β1/Smad signaling was possibly involved in the proliferation of neointima via modulation of TGF-β1/Smads signaling.
出处
《石河子大学学报（自然科学版）》
CAS
2014年第6期720-726,共7页
Journal of Shihezi University(Natural Science)
基金
国家自然科学基金项目(81160018)
新疆兵团博士资金专项(2014BB018)
石河子大学杰出青年培育计划(2013ZRKXJQ05)
