Viral myocarditis (VMC) is a common disease causing heart failure (HF) for which no specific treatments are available. As apoptosis of cardiomyoctes is a hallmark of VMC and HF, strategies targeting apoptosis are an effective way of prevention and treatment of HF. Recent studies found endoplasmic reticulum stress (ERS) reaction is a new signal transduction pathway mediating apoptosis. Calumenin protein (CP) is located within the endoplasmic reticulum Ca2+ binding proteins, and is important in ER-initiated apoptosis. The aim of this study was to investigate whether the function of CP was influenced in cardiomyocytes infected by coxsackievirus B3. The expression of CP was down-regulated in cardiomyocytes infected by coxsackievirus B3. TUNEL studies showed that apoptosis was increased in CP-deficient and ΔCP-mutant cardiomyocytes infected by coxsackievirus B3. Additionally, ERS-associated proteins (GRP78, p-PERK, p-eIF2α, ATF4 and CHOP) were up-regulated in coxsackievirus B3-infected CP-deficient and ΔCP-mutant cardiomyocytes compared to wild type control cells. These results suggested ER-initiated apoptosis was induced by coxsackievirus B3-infected cardiomyocytes and caused apoptosis through ER stress. CP can relieve ERS-initiated apoptosis in viral myocarditis.
Keywords: ERS-initiated apoptosis; Endoplasmic reticulum stress; calumenin protein; coxsackievirus B3; heart failure (HF).
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