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

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.

动脉粥样硬化（Atherosclerosis）是全球范围内最主要的致死性病因。本团队此前的研究表明，内皮细胞表面的热休克蛋白60（heat shock protein 60, HSP60）表达是引发该疾病的核心起始因素：该蛋白可作为T细胞自身抗原，且可被经典动脉粥样硬化危险因素所触发，此类危险因素涵盖感染（如肺炎衣原体（Chlamydia pneumoniae））、化学应激（吸烟、氧自由基、药物）、物理损伤（高温、血流剪切力）以及炎症反应（炎性细胞因子、脂多糖、氧化低密度脂蛋白、晚期糖基化终末产物）。在本研究中，我们证实氯化钠水平升高同样可诱导人脐静脉内皮细胞内及细胞表面的HSP60蛋白表达上调。此外，本研究还发现高钠环境会诱导细胞凋亡。