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中国应用生理学杂志 ›› 2017, Vol. 33 ›› Issue (4): 304-307.doi: 10.12047/j.cjap.5461.2017.074

• 研究论文 • 上一篇    下一篇

miRNA378*表达对柯萨奇B3病毒感染乳鼠心肌细胞凋亡、网腔钙结合蛋白、内质网应激伴侣蛋白表达的影响

赵明1, 刘晓翠2, 崔晓雪2, 邱祥春1, 王羽2,3, 魏成喜2,3   

  1. 1. 内蒙古民族大学第一临床医院, 通辽 028000;
    2. 内蒙古民族大学, 通辽 028000;
    3. 内蒙古民族大学医学院药物化学与药理学研究所, 通辽 028000
  • 收稿日期:2016-06-07 修回日期:2016-11-21 出版日期:2017-07-28 发布日期:2018-06-19
  • 通讯作者: 王羽,Tel:0475-8314234;E-mail:shen348@126.com;魏成喜,E-mail:weichengxi1224@163.com E-mail:shen348@126.com;weichengxi1224@163.com
  • 基金资助:
    内蒙古自治区自然科学基金(2015MS08153)

The correlation research on miRNA378* and calumenin,endoplasmic reticulum stress,apoptosis in suckling mouse myocardial cells infected with coxsackie virus B3

ZHAO Ming1, LIU Xiao-cui2, CUI Xiao-xue2, QIU Xiang-chun1, WANG Yu2,3, WEI Cheng-xi2,3   

  1. 1. The Inner-Mongolia National University First Clinical Hospital, Tongliao 028000, China;
    2. The Inner-Mongolia National University, Tongliao 028000, China;
    3. The Inner-Mongolia National University Medical Chemistry and Pharmacology Institute, Tongliao 028000, China
  • Received:2016-06-07 Revised:2016-11-21 Online:2017-07-28 Published:2018-06-19
  • Supported by:
    内蒙古自治区自然科学基金(2015MS08153)

摘要: 目的:研究沉默miRNA378*表达对柯萨奇B3病毒(CVB3)感染心肌细胞凋亡、内质网应激、网腔钙结合蛋白(calumenin)影响。方法:原代培养乳鼠心肌细胞分为:对照组(正常细胞)、柯萨奇病毒感染组(正常细胞+柯萨奇B3病毒)、miRNA378*沉默对照组(正常细胞+柯萨奇B3病毒+转染miRNA378*空质粒)、miRNA378*沉默组(正常细胞+柯萨奇B3病毒+转染miRNA378*沉默质粒),各组细胞分别转染和感染处理后置37℃、CO2培养箱中培养3 d。检测细胞α-平滑肌肌动蛋白(α-SMA)、细胞凋亡率、网腔钙结合蛋白、葡萄糖调节蛋白78(GRP78)及内质网应激信号通路因子激活转录因子6(ATF6)、转录因子C/EBP同源蛋白(CHOP)的表达。结果:通过检测ɑ-SMA蛋白,证实分离乳鼠细胞为心室肌细胞。TUNEL法检测不同组心室细胞凋亡情况发现,柯萨奇病毒感染组心室肌细胞凋亡明显,与柯萨奇病毒感染组心肌细胞相比较,miRNA378*沉默组心肌细胞凋亡细胞量明显减少。与柯萨奇病毒感染组比较,Calumenin表达减少(P<0.01),而GRP78、ATF6、CHOP表达增加(P<0.01)。结论:CVB3病毒感染心肌细胞作用与miRNA378*,引发内质网应激并激活信号通路因子,心肌细胞凋亡增加。

关键词: 心肌细胞, 乳鼠, miRNA378*, 柯萨奇B3病毒, 内质网应激, 网腔钙结合蛋白, 凋亡

Abstract: Objective: To investigate the effects of silencing miRNA378* on apoptosis, endoplasmic reticulum stress and calumenin of cardiomyocyte with coxsackie virus B3 (CVB3) infection.Methods: Primary cultured suckling mouse myocardium were divided into control group (normal cell), coxsackie virus infection group (normal cell and coxsackie virus B3), miRNA378* control group (normal cell +coxsackie virus B3+miRNA378* empty plasmid), miRNA378* silencing plasmid group(normal cells + coxsackie virus B3 + miRNA378* silencing plasmid). Four groups of cells were transfected, infected and treated in CO2 incubator at 37℃. The α-SMA protein, cell apoptosis rate, calumenin, glucose regulated protein 78 (GRP78), activation transcription factor 6(ATF6) and transcription factors c/ebp homologue protein (CHOP) in endoplasmic reticulum were analyzed.Results: By detecting α-SMA protein, the isolated suckling mouse ventricular myocardium were confirmed. TUNEL detection of different groups of ventricular cell apoptosis found that coxsackie virus group of ventricular myocytes apoptosis was significant. Compared with the coxsackie virus infection group of myocardial cells, miRNA378* silencing plasmid expression of cardiomyocyte apoptosis cells significantly reduced(P<0.01). The expressions of GRP78, ATF6 and CHOP were increased compared with those infected by Coxsackie virus infection (P<0.01), while the expressions of calumenin were decreased (P<0.01).Conclusion: CVB3 infected myocardial cells effected miRNA378* expression. It can trigger endoplasmic reticulum stress and activates signaling pathway factor and increase myocardial cell apoptosis.>

Key words: cardiomyocytes, suckling mice, miRNA378*, coxsackie virus B3, endoplasmic reticulum stress, calumenin, apoptosis

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