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    • Keywords


      microRNA-195; ischaemia–reperfusion; hypoxia/reoxygenation; cardiomyocyte apoptosis; Bcl-2; Bax; Cyt-c; caspase-3; caspase-9; mitochondrial membrane potentia.

    • Abstract


      This study aims to investigate microRNA-195 (miR-195) expression in myocardial ischaemia–reperfusion (I/R) injury andthe roles of miR-195 in cardiomyocyte apoptosis though targeting Bcl-2. A mouse model of I/R injury was established. MiR-195 expression levels were detected by real-time quantitative PCR (qPCR), and the cardiomyocyte apoptosis was detectedby TUNEL assay. After cardiomyocytes isolated from neonatal rats and transfected with miR-195 mimic or inhibitor, thehypoxia/reoxygenation (H/R) injury model was established. Cardiomyocyte apoptosis and mitochondrial membrane poten-tial were evaluated using flow cytometry. Bcl-2 and Bax mRNA expressions were detected by RT-PCR. Bcl-2, Bax andcytochrome c (Cyt-c) protein levels were determined by Western blot. Caspase-3 and caspase-9 activities were assessed byluciferase assay. Compared with the sham group, miR-195 expression levels and rate of cardiomyocyte apoptosis increasedsignificantly in I/R group (both P<0.05). Compared to H/R + negative control (NC) group, rate of cardiomyocyte apopto-sis increased in H/R + miR-195 mimic group while decreased in H/R + miR-195 inhibitor group (both P <0.05). MiR-195knockdown alleviated the loss of mitochondrial membrane potential (P <0.05). MiR-195 overexpression decreased Bcl-2mRNA and protein expression, increased BaxmRNA and protein expression, Cyt-c protein expression and caspase-3 andcaspase-9 activities (all P<0.05). While, downregulated MiR-195 increased Bcl-2 mRNA and protein expression, decreasedBax mRNA and protein expression, Cyt-c protein expression and caspase-3 and caspase-9 activities (all P <0.05). Ourstudy identified that miR-195 expression was upregulated in myocardial I/R injury, and miR-195 overexpression may promotecardiomyocyte apoptosis by targeting Bcl-2 and inducing mitochondrial apoptotic pathway.

    • Author Affiliations



      1. Department of Emergency, Longnan Hospital of Daqing, Daqing 163001, People’s Republic of China
      2. Department of Clinical Laboratory, Women and Children Hospital of Qingdao, Qingdao 266000, People’s Republic of China
      3. Department of Nephrology, the Affiliated Hospital to Changchun University of Chinese Medicine, Changchun 130000, People’s Republic of China
      4. Department of Laboratory, The First Hospital of YanTai, YanTai 261400, People’s Republic of China
    • Dates

  • Journal of Genetics | News

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