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J Cell Biochem. 2015 Oct;116(10):2365-74. doi: 10.1002/jcb.25187.

Heat Stress Induces Extended Plateau of Hsp70 Accumulation--A Possible Cytoprotection Mechanism in Hepatic Cells.

Author information

1
Department of Physiology and Biochemistry, Institute of Biology, Faculty of Natural Sciences and Mathematics, University "St Cyril and Methodius,", 1000, Skopje, Republic of Macedonia.
2
Departamento de Farmacolog, í, a, Facultad de Medicina- CIBERehd, Universidad de Valencia, Valencia, Spain.
3
FISABIO-Hospital Universitario Dr. Peset, Valencia, Spain.
4
Facultad de Ciencias de la Salud, Universitat Jaume I, Castell, o, n de la Plana, Spain.

Abstract

The relevance of heat preconditioning resides in its ability to protect cells from different kinds of injury by induction of heat shock proteins, a process in which the intensity of heat stress (HS) and duration of subsequent recovery are vital. This study evaluates the effects of moderate HS (45 min/43°C) and the time-dependent changes during recovery period of HSP70, Bcl-2 and p53 gene and protein expression in HepG2 cells. We also evaluated the effects of 0.4 mM aspirin (ASA) as a potential pharmacological co-inducer of HSP, both alone and in a combination with HS (ASA + HS). HS alone and ASA + HS caused a major up-regulation of HSP70 mRNA in the first 2 h, while HSP70 protein increased gradually and was especially abundant from 2 h to 24 h. Regarding Bcl-2, all treatments rendered similar results: gene expression was down-regulated in the first 2 h, after which there was protein elevation (12-48 h after HS). mRNA expression of p53 in HS- and (ASA + HS)-cells was down-regulated in the first 12 h. The immediate decrease of p53 protein after HS was followed by a biphasic increase. In conclusion, 0.4 mM ASA + HS does not act as a co-inducer of HSP70 in HepG2 cells, but promotes Bcl-2 protein expression during prolonged treatment. Our suggestion is that hepatic cells are most vulnerable in the first 2-6 h, but may have a high capacity for combating stress 12-24 h after HS. Finally, short-term exposure HS might be a "physiological conditioner" for liver cells to accumulate HSP and Bcl-2 proteins and thus obtain cytoprotection against an additional stress.

KEYWORDS:

ASPIRIN; HEAT PRECONDITIONING; HSP70; LIVER REGENERATION

PMID:
25857363
DOI:
10.1002/jcb.25187
[Indexed for MEDLINE]

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