血管内皮损伤后血管平滑肌细胞增殖的机制  

The mechanism of vascular smooth muscle cell (VSMC) proliferation after endothelial injury

作　　者：冯津萍[1] 陈星[1] 陈敏荔[1] 郭玉军[1] 梁爽霖[1] 

机构地区：[1]天津市胸科医院心内科,天津300051

出　　处：《中华急诊医学杂志》2005年第9期727-730,共4页Chinese Journal of Emergency Medicine

基　　金：天津市科技发展计划项目

摘　　要：目的探讨血管内皮损伤后血管平滑肌细胞增殖的机制。方法建立颈动脉血管内皮损伤的大鼠模型,行光镜和电镜观察;采用免疫组织化学法检测增殖细胞核抗原(PCNA)、I型胶原和IV型胶原;采用原位杂交法检测成纤维细胞生长因子(FGF)、血小板源生长因子(PDGF)、Bcl-2、Bax和c-myc的表达并行TUNEL染色。结果内皮损伤后血管管腔面积减少,平滑肌细胞(VSMC)增殖并呈激活状态细胞凋亡减少。PCNA、I型胶原、IV胶原、PDGF、FGF、Bcl-2和c-myc的表达增高,而Bax表达降低。结论血管内皮损伤后血管平滑肌细胞的迁移、增殖、凋亡及细胞外基质的分泌和堆积,受到多种细胞因子、生长因子和基因调控的介导,参与了局部血管重建和再塑过程。Objective To study the molecular mechanism of vascular smooth muscle cell （VSMC） proliferation after endothelial injury. Methods Endothelial injury of carotid artery was estalished in the rats. Type Ⅰ, Ⅳ collagen and proliferating cell nuclear antigen （PCNA） were examined by histoehemistry under electron microseope and light microscope. The mRNA expression of fibroblast growth factor （FGF）, platelet -derived growth factor （PDGF）, bel-2, bax and c-myc were determined by in situ hybridization. Results The vascular cavity area was significantly reduced, VSMC was activated and proliferated in the injured carotid artery. The expression of type Ⅰ, Ⅳ collagen, PCNA, FGF, PDGF, bcl-2 and c-myc mRNA were markedly induced, while bax mRNA was inhibited. Conclusion VSMC migration, proliferation, apoptosis and the deposition of extraeeilular matrix are mediated by several eytokines, growth factors and genes, thus participating in the process of vascular remodeling and revaseularization.

关 键 词：内皮损伤 平滑肌细胞 增殖 凋亡 血管平滑肌细胞增殖 血管内皮损伤 增殖细胞核抗原(PCNA) 成纤维细胞生长因子 血小板源生长因子 免疫组织化学法 

分 类 号：R363[医药卫生—病理学]