摘要
目的探讨CMTM3在肥厚性心肌病患者的心肌组织中的表达情况及肥厚性心肌病的发病机制。方法研究对象包括两部分:1)按每天15 mg/kg剂量腹腔注射异丙肾上腺素(ISO)诱导的心肌肥厚小鼠模型;2)2014年1月至2014年6月在阜外医院接受手术的肥厚性心肌病患者32例及3例正常心肌组织。使用半定量RT-PCR,realtime PCR及Western blot检测CMTM3在心肌组织转录和蛋白水平的表达。结果 1)在ISO诱导的心肌肥厚小鼠组织中,CMTM3 mRNA表达下调。2)在肥厚性心肌病患者病变的心肌组织中,CMTM3在转录水平和蛋白水平表达均下调。结论 CMTM3低表达致心肌组织增殖肥厚,可能参与了肥厚性心肌病发病。
Objective To investigate the expression of CMTM3 in human hypertophic myocardium,and the mechanism of hypertrophic cardiomyopathy.Methods The objects of this study consists of two parts：1） mouse model with cardiac hypertrophy induced by isoproterenol（ISO） injection with 15 mg/kg per day;2）32 cases of myocardial tissues from patients with hypertrophic cardiomypathy who were received surgery to clear the left ventricular outflow tract from January 2014 to June 2014 in Beijing Fuwai Cardiovascular Disease Hospital and 3 cases of normal myocardial tissues.RT-PCR,real-time PCR and Western blot were used to detect the expression of CMTM3 in protein and transcriptional levels.Results 1） Compared with the wild-type mice treated with normal saline,the expression of CMTM3 mRNA was down regulated.2） Compared to normal myocardium,the expression of CMTM3 was down regulated both in transciptional and protein level.Conclusions CMTM3 may play an important role in regulating the occurrence of hypertrophic cardiomypathy.
出处
《基础医学与临床》
CSCD
2015年第7期943-946,共4页
Basic and Clinical Medicine
基金
协和青年科研基金(2013-XHQN04-G)
