摘要
目的研究线粒体融合蛋白基因(mitofusion-2,Mfn2)促进大鼠血管平滑肌细胞(rVSMCs)凋亡的作用及其机制。方法以空载缺陷型腺病毒(Adv-GFP)为对照,以复制缺陷型腺病毒作为载体,将Mfn2转移到rVSMCs中,Western blot法观察感染后Mfn2基因的表达;TUNEL法检测凋亡细胞阳性率;琼脂糖凝胶电泳观察过表达Mfn2基因对细胞凋亡的影响;Western blot等检测凋亡相关因子Bcl-2、Bax和Caspase-9的含量。结果高表达Mfn2基因促进rVSMCs凋亡,使rVSMCs线粒体Bcl-2蛋白表达减少、Bax增多,胞质Caspases-9被激活。结论Mfn2基因促进rVSMCs的凋亡,其机制与活化线粒体凋亡途径有关。
Objective To investigate the effect of mitofusin-2 gene （Mfn2） on rat vascular smooth muscle cells （rVSMCs） apoptosis and the mechanism. Methods Mfn2 was delivered into rVSMCs by using replication-defective adenovirus as carriers and zero load adenovirus （Adv GFP） as controls. The morphological features of rVSMCs were observed by DeadEnd Colorimetric TUNEL system. The effect of Mfn2 overexpression on the apoptosis of rVSMCs was investigated by DNA ladder. The expression of Bcl-2, Bax and Caspase-9 was detected by using Western blot. Results Overexpression of Mfn2 gene promoted the apoptosis of rVSMCs, remarkably decreased the expression of mitochondrial Bcl-2 protein, decreased the expression of Bax and activated Caspases-9 after the rVSMCs were transfected with Mfn2. Conclusion Overexpression of rMfn2 gene triggers apoptosis of rVSMCs mediated by activation of the mitochondrial apoptotic pathway.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2007年第1期57-59,70,共4页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
国家自然科学基金资助项目(No.30570730)
