Open AccessElevated sodium leads to the increased expression of HSP60 and induces apoptosis in HUVECs
Author(s) -
Bojana Jakic,
Maja Buszko,
Giuseppe Cappellano,
Georg Wick
Publication year - 2017
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0179383
Subject(s) - hsp60 , heat shock protein , umbilical vein , lipopolysaccharide , glycation , inflammation , apoptosis , chemistry , oxidative stress , rage (emotion) , hsp70 , immunology , biology , biochemistry , receptor , neuroscience , in vitro , gene
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.