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
Abstract
Lei Zhang, Ming Liu, Hong Jiang, Ying Yu, Shuning Zhang, Jian Wu, Quan Cao, Peng Yu, Aijun Sun, Yunzeng Zou, Junbo Ge
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...
Key concepts: Pressure overload, HMGB1, Medicine, High-mobility group, Heart failure, Muscle hypertrophy, Cardiology, Internal medicine