2014CirculationRequires access

Abstract 11806: High-Mobility Group Box 1 Aggravates Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure

Lei Zhang, Ming Liu, Hong Jiang, Ying Yu, Shuning Zhang, Jian Wu, Quan Cao, Peng Yu, Aijun Sun, Yunzeng Zou, Junbo Ge

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Abstract

Introduction: Inflammatory response is involved in pressure overload-induced cardiac remodeling, but the mechanisms have not yet been fully elucidated. Hypothesis: High-mobility group box 1 (HMGB1), which is of crucial importance in inflammatory response, may participate in pressure overload-induced cardiac hypertrophy and heart failure. Methods: Pressure overload was imposed on the heart of adult male wild-type C57BL/6J mice by transverse aortic constriction (TAC), while 200ng recombinant HMGB1, HMGB1 box A (a competitive antagonist of HMGB1) or PBS was injected into the left ventricular wall. Transthoracic echocardiography, detection of proteins and genes expression in myocardium were performed at 2 and 4 weeks after the operation. Sections for histological analyses were generated from paraffin embedded hearts. Moreover, cardiac myocytes were cultured and given sustained mechanical stress and/or HMGB1 treatment before signaling pathways detection under the blockage of receptor for advanced glycation end...

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Introduction: Inflammatory response is involved in pressure overload-induced cardiac remodeling, but the mechanisms have not yet been fully elucidated. Hypothesis: High-mobility group box 1 (HMGB1), which is of crucial importance in inflammatory response, may participate in pressure overload-induced cardiac hypertrophy and heart failure. Methods: Pressure overload was imposed on the heart of adult male wild-type C57BL/6J mice by transverse aortic constriction (TAC), while 200ng recombinant HMGB1, HMGB1 box A (a competitive antagonist of HMGB1) or PBS was injected into the left ventricular wall. Transthoracic echocardiography, detection of proteins and genes expression in myocardium were performed at 2 and 4 weeks after the operation. Sections for histological analyses were generated from paraffin embedded hearts. Moreover, cardiac myocytes were cultured and given sustained mechanical stress and/or HMGB1 treatment before signaling pathways detection under the blockage of receptor for advanced glycation end...

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Available abstract

Introduction: Inflammatory response is involved in pressure overload-induced cardiac remodeling, but the mechanisms have not yet been fully elucidated. Hypothesis: High-mobility group box 1 (HMGB1), which is of crucial importance in inflammatory response, may participate in pressure overload-induced cardiac hypertrophy and heart failure. Methods: Pressure overload was imposed on the heart of adult male wild-type C57BL/6J mice by transverse aortic constriction (TAC), while 200ng recombinant HMGB1, HMGB1 box A (a competitive antagonist of HMGB1) or PBS was injected into the left ventricular wall. Transthoracic echocardiography, detection of proteins and genes expression in myocardium were performed at 2 and 4 weeks after the operation. Sections for histological analyses were generated from paraffin embedded hearts. Moreover, cardiac myocytes were cultured and given sustained mechanical stress and/or HMGB1 treatment before signaling pathways detection under the blockage of receptor for advanced glycation end...

Key concepts: Pressure overload, HMGB1, Medicine, High-mobility group, Heart failure, Muscle hypertrophy, Cardiology, Internal medicine

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Abstract 11806: High-Mobility Group Box 1 Aggravates Pressure Overload-Induced Cardiac Hypertrophy and Heart Failure — Research Paper | ScholarLens