粘着斑激酶在一氧化氮诱导血管平滑肌细胞凋亡中的作用  

Role of Focal Adhesion Kinase in Apoptosis of Rat Vascular Smooth Muscle Cells Induced by Nitric Oxide

作　　者：杨长春[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生物化学研究室,河北省石家庄市050017

出　　处：《中国动脉硬化杂志》2002年第1期10-12,共3页Chinese Journal of Arteriosclerosis

基　　金：国家自然科学基金(39970 2 74);河北省自然科学基金(30 1 358)资助

摘　　要：为研究一氧化氮对血管平滑肌细胞凋亡的影响及粘着斑激酶在一氧化氮诱导血管平滑肌细胞凋亡中的作用 ,应用脂多糖诱导血管平滑肌细胞合成内源性一氧化氮或加入可释放外源性一氧化氮的硝普钠 ,进行流式细胞术、DNA凝胶电泳及Northernblot和Westernblot分析。结果发现 ,无论是血管平滑肌细胞合成和释放的内源性一氧化氮还是体外补充的外源性一氧化氮均可显著诱导血管平滑肌细胞凋亡 ,且其诱导血管平滑肌细胞凋亡的强度与培养基中的NO-2 含量呈正相关 ;证实在一氧化氮诱导血管平滑肌细胞凋亡的同时 ,伴随Bcl 2和粘着斑激酶基因表达活性的明显下降。提示粘着斑激酶可能参与一氧化氮诱导血管平滑肌细胞凋亡的信号转导过程 ,一氧化氮诱导血管平滑肌细胞凋亡可能与抑制BclAim To investigate the effect of nitric oxide (NO) on the apoptosis of cultured rat vascular smooth muscle cells (VSMC) and the role of focal adhesion kinase (FAK) in VSMC apoptosis induced by NO. Methods Flow cytometry, DNA gel electrophoresis, Northern blot and Western blot were used to determine the effect of different level of NO on VSMC apoptosis and to explore the relationship between VSMC apoptosis and expression activity of Bcl 2 and FAK genes. Results The results showed that both endogenous NO synthesized by VSMC and exogenous NO released by sodium nitroprusside (SNP) could significantly induce apoptosis of cultured rat VSMC and the apoptosis rate of VSMC was correlated with NO content in the medium. It is demonstrated that the expression activity of Bcl 2 and FAK genes markedly decreased during apoptosis development of VSMC induced by NO. Conclusions It is suggested that FAK may be involved in signal conduction of VSMC apoptosis induced by NO, and VSMC apoptosis was related to down regulation of Bcl 2 and FAK expression.

关 键 词：粘着斑激酶 一氧化氮 细胞凋亡 流式细胞术 DMA凝胶电泳 NORTHERN BLOT WESTERN BLOT 密度扫描 血管平滑肌细胞 Bcl-2 

分 类 号：R322.12[医药卫生—人体解剖和组织胚胎学]