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高钠会导致HSP60表达增加并诱导人脐静脉内皮细胞凋亡。

Elevated sodium leads to the increased expression of HSP60 and induces apoptosis in HUVECs.

作者信息

Jakic Bojana, Buszko Maja, Cappellano Giuseppe, Wick Georg

机构信息

Laboratory of Autoimmunity, Division of Experimental Pathophysiology and Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.

出版信息

PLoS One. 2017 Jun 12;12(6):e0179383. doi: 10.1371/journal.pone.0179383. eCollection 2017.

Abstract

Atherosclerosis is the leading cause of death in the world. We have previously shown that expression of heat shock protein 60 (HSP60) on the surface of endothelial cells is the main cause of initiating the disease as it acts as a T cell auto-antigen and can be triggered by classical atherosclerosis risk factors, such as infection (e.g. Chlamydia pneumoniae), chemical stress (smoking, oxygen radicals, drugs), physical insult (heat, shear blood flow) and inflammation (inflammatory cytokines, lipopolysaccharide, oxidized low density lipoprotein, advanced glycation end products). In the present study, we show that increasing levels of sodium chloride can also induce an increase in intracellular and surface expression of HSP60 protein in human umbilical vein endothelial cells. In addition, we found that elevated sodium induces apoptosis.

摘要

动脉粥样硬化是全球主要的死亡原因。我们之前已经表明,内皮细胞表面热休克蛋白60(HSP60)的表达是引发该疾病的主要原因,因为它作为一种T细胞自身抗原,可由经典的动脉粥样硬化危险因素触发,如感染(如肺炎衣原体)、化学应激(吸烟、氧自由基、药物)、物理损伤(热、剪切血流)和炎症(炎性细胞因子、脂多糖、氧化型低密度脂蛋白、晚期糖基化终产物)。在本研究中,我们表明氯化钠水平的升高也可诱导人脐静脉内皮细胞中HSP60蛋白的细胞内和表面表达增加。此外,我们发现钠升高会诱导细胞凋亡。

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