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首页> 外文期刊>Journal of cellular and molecular medicine. >Extracellular high‐mobility group box 1 mediates pressure overload‐induced cardiac hypertrophy and heart failure
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Extracellular high‐mobility group box 1 mediates pressure overload‐induced cardiac hypertrophy and heart failure

机译：细胞外高迁移率分组框1介导压力超负荷引起的心脏肥大和心力衰竭

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摘要

Inflammation plays a key role in pressure overload-induced cardiac hypertrophy and heart failure, but the mechanisms have not been fully elucidated. High-mobility group box 1 (HMGB1), which is increased in myocardium under pressure overload, may be involved in pressure overload-induced cardiac injury. The objectives of this study are to determine the role of HMGB1 in cardiac hypertrophy and cardiac dysfunction under pressure overload. Pressure overload was imposed on the heart of male wild-type mice by transverse aortic constriction (TAC), while recombinant HMGB1, HMGB1 box A (a competitive antagonist of HMGB1) or PBS was injected into the LV wall. Moreover, cardiac myocytes were cultured and given sustained mechanical stress. Transthoracic echocardiography was performed after the operation and sections for histological analyses were generated from paraffin-embedded hearts. Relevant proteins and genes were detected. Cardiac HMGB1 expression was increased after TAC, which was accompanied by its translocation from nucleus to both cytoplasm and intercellular space. Exogenous HMGB1 aggravated TAC-induced cardiac hypertrophy and cardiac dysfunction, as demonstrated by echocardiographic analyses, histological analyses and foetal cardiac genes detection. Nevertheless, the aforementioned pathological change induced by TAC could partially be reversed by HMGB1 inhibition. Consistent with the in vivo observations, mechanical stress evoked the release and synthesis of HMGB1 in cultured cardiac myocytes. This study indicates that the activated and up-regulated HMGB1 in myocardium, which might partially be derived from cardiac myocytes under pressure overload, may be of crucial importance in pressure overload-induced cardiac hypertrophy and cardiac dysfunction.
机译：炎症在压力超负荷引起的心脏肥大和心力衰竭中起关键作用，但其机制尚未完全阐明。在压力超负荷下心肌中增加的高迁移率分组盒1（HMGB1）可能与压力超负荷引起的心脏损伤有关。这项研究的目的是确定HMGB1在压力超负荷下在心肌肥大和心脏功能障碍中的作用。通过横向主动脉收缩（TAC）对雄性野生型小鼠的心脏施加压力超负荷，同时将重组HMGB1，HMGB1 box A（HMGB1的竞争性拮抗剂）或PBS注入LV壁。此外，培养心肌细胞并给予持续的机械应力。手术后进行胸腔超声心动图检查，并从石蜡包埋的心脏中产生组织学分析切片。检测到相关的蛋白质和基因。 TAC后心脏HMGB1表达增加，并伴有其从细胞核到细胞质和细胞间空间的易位。超声心动图分析，组织学分析和胎儿心脏基因检测证明，外源性HMGB1加重了TAC诱导的心脏肥大和心脏功能障碍。然而，由TAC诱导的上述病理变化可以被HMGB1抑制部分逆转。与体内观察一致，机械应力引起HMGB1在培养的心肌细胞中的释放和合成。这项研究表明，心肌中HMGB1的激活和上调可能部分来自压力超负荷下的心肌细胞，在压力超负荷引起的心脏肥大和心脏功能障碍中可能至关重要。

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