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Cardiac Myocyte Mechanics and Myosin Heavy Chain Gene Expression in Cultured Myocytes Infected with Coxsackievirus B_3

Wan Chao

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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.

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Available 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.

Key concepts: Myocyte, Coxsackievirus, Contractility, Myosin, Cardiac myocyte, Biology, Myosin light-chain kinase, Internal medicine

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