Diet-induced elevation of circulating HSP70 may trigger cell adhesion and promote the development of atherosclerosis in rats

Although accumulating evidence indicates that heat shock protein 70 (HSP70) could be secreted into plasma and its levels have been found to have an ambiguous association with atherosclerosis, our knowledge for the exact role of circulating HSP70 in the development of atherosclerosis is still limited...

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Bibliographic Details
Published in:Cell stress & chaperones 2016-09, Vol.21 (5), p.907-914
Main Authors: Xie, Fang, Zhan, Rui, Yan, Li-Cheng, Gong, Jing-Bo, Zhao, Yun, Ma, Jing, Qian, Ling-Jia
Format: Article
Language:English
Subjects:
Animals
Antibodies
Atherosclerosis
Atherosclerosis - blood
Atherosclerosis - etiology
Biochemistry
Biomedical and Life Sciences
Biomedicine
Blood
Blood plasma
Cancer Research
Cell Adhesion
Cell Biology
Cell Survival
Cells, Cultured
Cultured cells
Cytokines
Diet, High-Fat - adverse effects
Endothelial cells
Endothelial Cells - physiology
Heat shock proteins
HSP70 Heat-Shock Proteins - blood
Immunology
Interleukin-6 - metabolism
Lipoproteins, LDL - blood
Male
Monocytes
Monocytes - metabolism
Neurosciences
Original Paper
Rats, Sprague-Dawley
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Summary:Although accumulating evidence indicates that heat shock protein 70 (HSP70) could be secreted into plasma and its levels have been found to have an ambiguous association with atherosclerosis, our knowledge for the exact role of circulating HSP70 in the development of atherosclerosis is still limited. In the present study, we report an adhesion-promoting effect of exogenous HSP70 and evaluate the potential involvement of elevated circulating HSP70 in the development of atherosclerosis. Time-dependent elevation of plasma HSP70 was found in diet-induced atherosclerotic rats, whose effect was investigated through further in vitro experiments. In rat aortic endothelial cell (RAEC) cultures, exogenous HSP70 incubation neither produced cell injuries by itself nor had protective effects on cell injuries caused by Ox-LDL or homocysteine. However, exogenous HSP70 administration could lead to a higher adhesion rate between rat peripheral blood monocytes (PBMCs) and RAECs. This adhesion-promoting effect appeared only when PBMCs, rather than RAECs, were pretreated with HSP70 incubation. PBMCs in an HSP70 environment released more IL-6 to supernatant, which subsequently up-regulated the expression of ICAM-1 in RAECs. These results indicate that the diet-induced elevation of circulating HSP70 could trigger cell adhesion with the help of IL-6 as a mediator, which provides a novel possible mechanism for understanding the role of circulating HSP70 in the pathogenesis of atherosclerosis.
ISSN:1355-8145
1466-1268
DOI:10.1007/s12192-016-0716-2