SM22α抑制大鼠基质重构相关分子的表达及其在血管肥厚中的意义  

SM22α inhibits expression of matrix remodeling-related molecules and vascular hypertrophy in rats

作　　者：王晓娟[1] 吕品[1] 韩梅[1] 

机构地区：[1]河北医科大学基础医学院生物化学与分子生物学教研室,河北省医学生物技术重点实验室,神经与血管省部共建教育部重点实验室,河北石家庄050017

出　　处：《中国病理生理杂志》2013年第12期2113-2120,共8页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.31071003;No.31271222);国家国际科技合作专项(No.2011DFA32700)

摘　　要：目的:探讨平滑肌蛋白22α(smooth muscle protein 22 alpha,SM22α)对大鼠血管肥厚及基质重构相关分子表达的影响。方法:采用SM22α及其突变体的腺病毒表达载体感染大鼠颈总动脉;利用血管紧张素II(angiotensin II,Ang II)微渗泵植入大鼠皮下复制高血压模型;用HE及免疫组化方法分别观察大鼠颈总动脉肥厚及基质重构相关分子在血管壁的表达情况。结果:Ang II显著升高大鼠的血压;颈总动脉过表达SM22α及其非磷酸化突变体S181A后,显著抑制Ang II诱导的血管肥厚,同时伴有MMP-2、MMP-9、ICAM-1和VCAM-1的表达减少。结论:SM22α及其非磷酸化突变体显著抑制血管肥厚,该过程可能与其抑制基质重构相关的MMP及黏附分子的表达有关。[ ABSTRACT J AIM ： To investigate the effect of smooth muscle protein 22 alpha （5M22et） on the vascular hyper- trophy and the expression of matrix remodeling-related molecules in rats. METHODS ： Rat carotid arteries were infected with adenovirus, Ad-GFP-SM22et, Ad-GFP-S181 D or Ad-GFP-S181A. Two days later, the rats were re-anesthetized and osmotic minipumps were subcutaneously implanted for angiotensin II （Ang II） infusion. The carotid arteries were analyzed using HE staining and the method of immunohistochemistry. RESULTS ： Systolic blood pressure significantly increased in the rats receiving Ang II. The vascular medial thickness had a marked increase after Ang II infusion, and was inhibited by the over-expression of SM22ot and S181A mutant （inhibition of SM22ot phosphorylation）. Furthermore, the expression of MMP-2, MMP-9, ICAM-1 and VCAM-1 was also inhibited by SM22c~ and S181A over-expression. CONCLUSION： Over-expression of SM22ct and S181A mutant inhibits vascular hypertrophy, which is associated with the down-regulation of the matrix remodeling-related molecules MMP-2, MMP-9, ICAM-1 and VCAM-1.

关 键 词：平滑肌蛋白22α 血管肥厚 黏附分子 基质金属蛋白酶类 血管紧张素Ⅱ 

分 类 号：R34[医药卫生—基础医学]