Li Xiaoou, Xie Lili, He Bing, Huang Wei
Department of Newborn, People's Hospital, Wuhan University, Wuhan 430060, China. *Corresponding author, E-mail:
Department of Newborn, People's Hospital, Wuhan University, Wuhan 430060, China.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2018 Jan;34(1):41-46.
Objective To study the role of a disintegrin and metalloproteinase10 (ADAM10) in shedding neural cadherin (N-cadherin) and develop an approach to interfere the process of ventricular remodeling in adriamycin-induced cardiomyopathy (ACM) rats. Methods In a rat model of ACM, the effects of intraperitoneal injection of the lentiviral RNAi vector of ADAM10 on the morphology of cardiomyocytes and contractile function were observed by HE staining and color Doppler echocardiography. The expressions of N-cadherin and C-terminal fragment 1 (CTF1) were detected by Western blotting and immunohistochemistry. Results In the in vivo experiment, a large amount of fluorescence was seen in the isolated primary cardiomyocytes, which indicated that the transfection in the rat model was successful. In the treatment group, the morphology of cardiomyocytes and function of the heart were evidently improved, N-cadherin protein expression was remarkably up-regulated and CTF1 protein was obviously down-regulated compared with the model group. Conclusion Knock-down of ADAM10 increases N-cadherin expression and decreases CTF1 expression, thus improves cardiac function in the rat model of ACM.
目的 研究解整合素金属蛋白酶10（ADAM10）在神经钙黏蛋白（N-cadherin）脱落中的作用，并探索一种干预阿霉素诱导的心肌病（ACM）大鼠心室重塑过程的方法。方法 在ACM大鼠模型中，通过HE染色和彩色多普勒超声心动图观察腹腔注射ADAM10慢病毒RNAi载体对心肌细胞形态和收缩功能的影响。采用蛋白质印迹法和免疫组织化学法检测N-cadherin和C末端片段1（CTF1）的表达。结果 在体内实验中，分离的原代心肌细胞中可见大量荧光，表明大鼠模型转染成功。与模型组相比，治疗组心肌细胞形态和心脏功能明显改善，N-cadherin蛋白表达显著上调，CTF1蛋白明显下调。结论 敲低ADAM10可增加N-cadherin表达，降低CTF1表达，从而改善ACM大鼠模型的心脏功能。
