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