瞬时受体电位通道A1在压力负荷致心肌肥厚小鼠的表达及意义  

Expression of transient receptor potential channel A1 and its significance in pressure overload-induced cardiac hypertrophy mice

作　　者：王震[1] 刘剑芳[1] 王梦龙[1] 叶晶[1] 徐瑶[1] 姜慧敏[1] 叶迪 万军[1] Wang Zhen;Liu Jianfang;Wang Menglong;Ye Jing;Xu Yao;Jiang Huimin;Ye Di;Wan Jun(Department of Cardiology,Wuhan University People＇s Hospital,Wuhan University Cardiovascular Disease Institute,Hubei Provincial Key Laboratory of Cardiovascular Disease,Wuhan 430060,Hebei Province,China)

机构地区：[1]武汉大学人民医院心血管内科武汉大学心血管病研究所心血管病湖北省重点实验室,430060

出　　处：《中华老年心脑血管病杂志》2018年第8期858-861,共4页Chinese Journal of Geriatric Heart,Brain and Vessel Diseases

基　　金：国家自然科学基金(81170208)

摘　　要：目的探讨瞬时受体电位通道A1(TRPA1)在压力负荷致心肌肥厚小鼠心肌组织中的表达及意义。方法选择SPF级雄性小鼠32只,随机分为假手术组和模型组,每组各16只。2组于第4周行超声检测,包括左心室收缩末期内径(LVESD)、左心室舒张末期内径(LVEDD)、LVEF以及左心室短轴缩短率(LVFS)。处死小鼠测量心脏质量和体质量,常规心肌组织苏木精伊红染色和麦胚凝集素染色。RT-PCR检测小鼠心肌组织心房钠尿肽(ANP)、心肌肌球蛋白重链β(β-MHC)和TRPA1mRNA表达,Western blot检测小鼠心肌组织磷酸化钙调蛋白依赖性的蛋白激酶Ⅱ(CaMKⅡ)、总CaMKⅡ和TRPA1蛋白表达。结果模型组小鼠心脏质量、LVESD和LVEDD明显高于假手术组,LVEF和LVFS明显低于假手术组(P<0.05)。模型组小鼠心肌细胞横截面积明显高于假手术组[(389.4±46.3)μm2 vs(213.1±27.5)μm2,P<0.05]。与假手术组比较,模型组小鼠心肌组织ANP、β-MHC和TRPA1mRNA表达明显上调(P<0.01);模型组小鼠心肌组织磷酸化CaMKⅡ/总CaMKⅡ和TRPA1蛋白表达明显升高(P<0.01)。结论 TRPA1参与致心肌肥厚的过程,其机制可能与Ca2+相关信号相关。Objective To study the expression of TRPA1 and its significance in pressure overloadinduced cardiac hypertrophy mice.Methods Thirty-two male mice were divided into sham-operation group（n=16）and model group（n=16）.The cardiac functional indexes of mice（LVESD,LVEDD,LVEF and LVFS）were detected by echocardiography in two groups at week 4.The animals were sacrificed and tissue samples were taken for the measurement of their heart weight and body weight with HE and wheat germ agglutinin staining.The expressions of ANP,β-MHC and TRPA1 mRNA in mouse myocardium were detected by RT-PCR,and those of p-CaMKⅡ,total CaMKⅡand TRPA1 protein in mouse myocardium were detected by Western blot.Results The heart weight was significantly heavier,the LVESD and LVEDD were significantly longer,the LVEF and LVFS were significantly higher in model group than in sham-operation group.The cross-sectional area of cardiomyocytes was significantly larger in model group than in sham-operation group（389.4±46.3μm2 vs 213.1±27.5μm2,P〈0.05）.The expression levels of ANP,β-MHC,TRPA1 mRNA,p-CaMKⅡ,and TRPA1 protein in mouse myocardium were significantly higher in model group than in sham-operation group（P〈0.01）.Conclusion TRPA1 is involved in myocardial hypertrophy and its mechanism is related with the Ca2＋relevant signals.

关 键 词：瞬时受体电位通道 心肌病 肥厚性 心钠素 肌球蛋白重链 

分 类 号：R542.2[医药卫生—心血管疾病]