机构地区:[1]Department of Cardiology,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology [2]Division of Clinics,Tonji Medical College,Huazhong University of Science and Technology
出 处:《Journal of Huazhong University of Science and Technology(Medical Sciences)》2010年第5期582-588,共7页华中科技大学学报(医学英德文版)
基 金:supported by a grant from National Key Basic Research Program of China (No.2007CB512000,Sub-Project No.2007CB512005)
摘 要:Autoimmune is involved in the pathogenesis of ventricular remodeling in acute myocardial infarction (AMI).In the present study, we investigated the effect of anti-cardiac myosin heavy chain antibodies (AMHCA) from patients with AMI on rat cardiomyocyte apoptosis.Cardiomyocyte apoptosis was observed and measured by DNA end labeling and Annexin-Ⅴ/PI double-staining assay.The expression of apoptosis related p53 and Bcl-2 protein and the second messenger calcium were detected respectively by Western blotting, patch clamp and confocal calcium imaging.The results showed that AMHCA was able to induce cardiomyocyte apoptosis in a dose dependent manner.Apoptosis-accelerating nucleoprotein p53 was up-regulated, while apoptosis-inhibiting cytoplasmic protein Bcl-2 was down-regulated.In parallel, cytoplasmic calcium concentration was elevated.There was no effect on L-type calcium currents.It is concluded that AMHCA in patients with AMI as a novel triggering factor can induce cardiomyocyte apoptosis, which contributes to ventricular remodeling.Autoimmune is involved in the pathogenesis of ventricular remodeling in acute myocardial infarction (AMI).In the present study, we investigated the effect of anti-cardiac myosin heavy chain antibodies (AMHCA) from patients with AMI on rat cardiomyocyte apoptosis.Cardiomyocyte apoptosis was observed and measured by DNA end labeling and Annexin-Ⅴ/PI double-staining assay.The expression of apoptosis related p53 and Bcl-2 protein and the second messenger calcium were detected respectively by Western blotting, patch clamp and confocal calcium imaging.The results showed that AMHCA was able to induce cardiomyocyte apoptosis in a dose dependent manner.Apoptosis-accelerating nucleoprotein p53 was up-regulated, while apoptosis-inhibiting cytoplasmic protein Bcl-2 was down-regulated.In parallel, cytoplasmic calcium concentration was elevated.There was no effect on L-type calcium currents.It is concluded that AMHCA in patients with AMI as a novel triggering factor can induce cardiomyocyte apoptosis, which contributes to ventricular remodeling.
关 键 词:AUTOANTIBODY cardiac myosin heavy chain apoptosis p53 Bcl-2 CALCIUM
分 类 号:R542.22[医药卫生—心血管疾病]
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