KLF4抑制球囊损伤诱导的新生内膜形成  

Exogenous KLF4 inhibits neointimal hyperplasia after balloon injury in rat

作　　者：赵欣铭[1] 董丽华[1] 孟芳[1] 郑斌[1] 温进坤[1] 韩梅[1] 

机构地区：[1]河北医科大学基础医学研究所,河北省医学生物技术重点实验室,河北石家庄050017

出　　处：《中国病理生理杂志》2009年第7期1303-1306,共4页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30770787);河北省自然科学基金资助项目(No.C2008001049)

摘　　要：目的:通过腺病毒载体介导外源性KLF4在大鼠颈动脉球囊剥脱血管中进行表达,观察新生内膜增生情况,研究外源性KLF4对球囊损伤诱导的新生内膜形成的影响及初步探讨其机制。方法:构建含有KLF4基因的重组腺病毒载体pAd-KLF4,将其导入内皮剥脱的血管壁。用HE染色观察血管新生内膜的厚度,免疫组织化学染色和RT-PCR分别检测外源性KLF4在血管中的表达以及与增殖和分化标志基因表达的关系。结果:重组腺病毒pAd-KLF4可在血管壁中稳定表达KLF4。KLF4的过表达可显著抑制球囊损伤后血管新生内膜的增厚,转染pAd-KLF4的血管,其内膜/中膜比值(I/M)(0.52±0.15)明显小于pAd对照组(2.48±0.38),P<0.05。pAd-KLF4组血管壁增殖标志蛋白PCNA和c-Jun表达也较pAd组明显降低(P<0.05)。结论:KLF4过表达可阻断损伤诱导的血管平滑肌细胞表型转化,进而抑制球囊剥脱后血管内膜的增生。AIM： To observe the neointimal hyperplasia and to investigate the effect and mechanism of exogenous kruppel - like factor 4 （ KLF4 ） on neointimal formation induced by balloon injury. METHODS ： Adenovirus vector encoding the KLF4 （pAd -KLF4） was constructed and transfected into the balloon -injured carotid artery in rat. Neointima thickening was assessed using HE staining. Expression of exogenous KLF4 and the marker genes were detected by immunohistochemistry and RT - PCR. RESULTS： pad - KLF4 stably expressed KLF4 protein in the transfected vascular wall. Overexpression of KLF4 significantly inhibited neointimal hyperplasia induced by balloon injury. The ratio of intima - to - media area （I/M） in pAd - KLF4 group （2.48 ±0. 38） was significantly less than that in pad group （0. 52 ±0. 15） （ P 〈 0. 05 ）. Proliferating cell nuclear antigen （PCNA） and c - Jun were significantly reduced in pAd - KLF4 group, compared with the pad group （ P 〈 0. 05 ）. CONCLUSION： Overexpression of KLF4 inhibits the phenotype remodeling of vascular smooth muscle cells and neointimal hyperplasia induced by balloon injury.

关 键 词：Krppel样因子 腺病毒载体 气囊损伤 新生内膜 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学]