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CARDIAC MYOCYTE MECHANICS AND GENE EXPRESSION OF MYOCARDIAL CONTRACTILEPROTEIN IN VITROAUTOIMMUNE MECHANISM CAUSED BY COXSACKIVIRUS B3

Chaomin Wan

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Abstract

The mechanism of cell-mediated antoimmune response of cardiac myocyte to coxsackievirus B3 was studied by setting up cellular model of cell-mediated autoimmune injuring myocytes after affected by coxsackivevirus B3(CVB3), then cardiac myocyte mechanics were analyzed and gene expression of the myocardial contractile proteins, α-myosin heavy chain (α-MHC), β-myosin heavy chain (β-MHC) were measured. Results showed that cell-mediated autoimmune response to coxsackivevirus B3 led to damage of cultured cardiac myocytes after incubated with the white blood cells infected by CVB3. The myocyte contractility in immune damaged cardiac myocytes was significantly lower than in normal myocytes(P0.01). The decrease in myocyte contractility at 24 hours after inducing immunized white blood cells was greater than that at 12 hours. The gene expression level of mRNA for the myocardial contractile protein, α-MHC, was significantly lower in cardiac myocytes after culture with inducing immunized white blood cell (0.0575±0.005) than in normal myocytes (0.1829±0.023). However, the mRNA level forβ-MHC was significantly higher (0.1015±0.001) after inducing immunized white blood cell than in normal myocytes(0.0872±0.005).

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The mechanism of cell-mediated antoimmune response of cardiac myocyte to coxsackievirus B3 was studied by setting up cellular model of cell-mediated autoimmune injuring myocytes after affected by coxsackivevirus B3(CVB3), then cardiac myocyte mechanics were analyzed and gene expression of the myocardial contractile proteins, α-myosin heavy chain (α-MHC), β-myosin heavy chain (β-MHC) were measured. Results showed that cell-mediated autoimmune response to coxsackivevirus B3 led to damage of cultured cardiac myocytes after incubated with the white blood cells infected by CVB3. The myocyte contractility in immune damaged cardiac myocytes was significantly lower than in normal myocytes(P0.01). The decrease in myocyte contractility at 24 hours after inducing immunized white blood cells was greater than that at 12 hours. The gene expression level of mRNA for the myocardial contractile protein, α-MHC, was significantly lower in cardiac myocytes after culture with inducing immunized white blood cell (0.0575±0.005) than in normal myocytes (0.1829±0.023). However, the mRNA level forβ-MHC was significantly higher (0.1015±0.001) after inducing immunized white blood cell than in normal myocytes(0.0872±0.005).

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Available abstract

The mechanism of cell-mediated antoimmune response of cardiac myocyte to coxsackievirus B3 was studied by setting up cellular model of cell-mediated autoimmune injuring myocytes after affected by coxsackivevirus B3(CVB3), then cardiac myocyte mechanics were analyzed and gene expression of the myocardial contractile proteins, α-myosin heavy chain (α-MHC), β-myosin heavy chain (β-MHC) were measured. Results showed that cell-mediated autoimmune response to coxsackivevirus B3 led to damage of cultured cardiac myocytes after incubated with the white blood cells infected by CVB3. The myocyte contractility in immune damaged cardiac myocytes was significantly lower than in normal myocytes(P0.01). The decrease in myocyte contractility at 24 hours after inducing immunized white blood cells was greater than that at 12 hours. The gene expression level of mRNA for the myocardial contractile protein, α-MHC, was significantly lower in cardiac myocytes after culture with inducing immunized white blood cell (0.0575±0.005) than in normal myocytes (0.1829±0.023). However, the mRNA level forβ-MHC was significantly higher (0.1015±0.001) after inducing immunized white blood cell than in normal myocytes(0.0872±0.005).

Key concepts: Myocyte, Contractility, Cardiac myocyte, Internal medicine, Myosin, Endocrinology, Biology, Medicine

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