Cardiac Myocyte Mechanics and Myosin Heavy Chain Gene Expression in Cultured Myocytes Infected with Coxsackievirus B_3
Wan Chao
Abstract
Wan Chao
Abstract
Objective To determine the mechanisms of direct virus injury to cardiac myocytes. Method Cardiac myocyte mechanics and gene expression of the myocardial contractile proteins α myosin heavy chain(α MHC) and β myosin heavy chain (β MHC)in normal cardiac myocytes Coxsackievirus B 3 were analysed. Result Contractility was significantly lower in infected cardiac myocytes than in normal cardiac myocytes(P 0.01 ). The decrease in contractility was more significant at 24 h than at 12 h after infection(P0.05). The level of mRNA for myocardial contractile protein α MHC was significantly lower in cardiac myocytes(0.1274) infected with Coxsackievirus B 3 than in normal myocytes(0.1529).However, the mRNA level for β MHC was significantly higher in infected myocytes(0.1108) than in normal myocytes(0.0872). Conclusion Myocyte contractility may be reduced because the infection with Coxsackievirus B 3 may affect gene expression of myocyte contractile proteins; viral injury may cause a shift of protein expression from preponderance of α MHC to prepouderance of β MHC.
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Objective To determine the mechanisms of direct virus injury to cardiac myocytes. Method Cardiac myocyte mechanics and gene expression of the myocardial contractile proteins α myosin heavy chain(α MHC) and β myosin heavy chain (β MHC)in normal cardiac myocytes Coxsackievirus B 3 were analysed. Result Contractility was significantly lower in infected cardiac myocytes than in normal cardiac myocytes(P 0.01 ). The decrease in contractility was more significant at 24 h than at 12 h after infection(P0.05). The level of mRNA for myocardial contractile protein α MHC was significantly lower in cardiac myocytes(0.1274) infected with Coxsackievirus B 3 than in normal myocytes(0.1529).However, the mRNA level for β MHC was significantly higher in infected myocytes(0.1108) than in normal myocytes(0.0872). Conclusion Myocyte contractility may be reduced because the infection with Coxsackievirus B 3 may affect gene expression of myocyte contractile proteins; viral injury may cause a shift of protein expression from preponderance of α MHC to prepouderance of β MHC.
Key concepts: Myocyte, Coxsackievirus, Contractility, Myosin, Cardiac myocyte, Biology, Myosin light-chain kinase, Internal medicine