Dysbindin转基因小鼠心肌肥厚模型中基因变化  

The gene changes in Dysbindin transgenic mice model of cardiac hypertrophy

作　　者：蒋珍妮[1] 朱国能 王迎超 赵文胜[2] Jiang Zhenni

机构地区：[1]浙江大学医学院附属第二医院,310008 [2]浙江省中西医结合医院,310003 [3]浙江大学药学院,310030

出　　处：《浙江临床医学》2022年第3期350-352,共3页Zhejiang Clinical Medical Journal

基　　金：浙江省基础公益研究计划项目(2018C37117)。

摘　　要：目的探讨Dysbindin转基因小鼠不同心肌肥厚模型心肌肥厚标志基因的表达。方法构建cTNT-Dysbindin-IRES-EGFP-polyA质粒,受精卵原核显微注射C57BL/6小鼠,建立Dysbindin转基因小鼠。采用异丙肾上腺素(Isoprotemol,ISO)和胸主动脉缩窄(Thoracic aorta constriction,TAC)诱导心肌肥厚。造模结束,称取小鼠体重、心脏重量,计算心脏重量指数(HW/BW);采用qRT-PCR检测心肌肥厚标志基因表达。结果应用PCR扩增产物和GFP阳性验证Dysbindin转基因小鼠特异性表达在心肌。ISO组和TAC组转基因小鼠和野生型小鼠的HW/BW和心肌肥厚标志基因升高,与野生型小鼠比较,转基因小鼠心房利钠肽(ANP)和-肌球蛋白重链(-MHC)基因表达水平降低。结论Dysbindin转基因小鼠对于ISO和TAC诱导心肌肥厚有减轻作用,ANP和-MHC降低优于脑钠钛(BNP)。Objective To explore the expression of myocardial hypertrophy marker genes in Dysbindin transgenic mice different models of myocardial hypertrophy.Methods Construct cTNT-Dysbindin-IRES-EGFP-polyA plasmid,and establish Dysbindin transgenic by microinjecting into zygote pronuclei of C57BL/6 mice.Isoprotemol(ISO)and Thoracic aorta constriction(TAC)respectively were used to induce the mode of myocardial hypertrophy.After modeling,each mouse's weight and heart weight were weighed,and the heart weight index(HW/BW)were calculated;the expression of myocardial hypertrophy marker genes was detected by qRT-PCR.Results The Dysbindin specific expression in myocardium of transgenic mouse was verified by PCR amplification products and positive GFP.HW/BW and the expression of myocardial hypertrophy marker genes were elevated in transgenic mice and wild-type mice in both ISO and TAC groups,and the expression levels of ANP and β-MHC genes in transgenic mice were reduced compared with those in wild-type mice.Conclusion Dysbindin transgenic mice have a mitigating effect on ISO and TAC-induced myocardial hypertrophy,and reductions in ANP and β-MHC more than in BNP.

关 键 词：DYSBINDIN 转基因 心肌肥厚 标志基因 

分 类 号：R54[医药卫生—心血管疾病]