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Heat Stress Induces Extended Plateau of Hsp70 Accumulation – A Possible Cytoprotection Mechanism in Hepatic Cells
dc.contributor.author | Miova, Biljana | |
dc.contributor.author | Dinevska-Kjovkarovska, Suzana | |
dc.contributor.author | Esplugues Mota, Juan V. | |
dc.contributor.author | Apostolova, Nadezda | |
dc.date.accessioned | 2016-09-23T07:54:02Z | |
dc.date.available | 2016-09-23T07:54:02Z | |
dc.date.issued | 2015-08-15 | |
dc.identifier.citation | MIOVA, Biljana, et al. Heat Stress Induces Extended Plateau of Hsp70 Accumulation–A Possible Cytoprotection Mechanism in Hepatic Cells. Journal of cellular biochemistry, 2015, vol. 116, no 10, p. 2365-2374 | ca_CA |
dc.identifier.uri | http://hdl.handle.net/10234/162868 | |
dc.description.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. J. Cell. Biochem. 116: 2365–2374, 2015. © 2015 Wiley Periodicals, Inc. | ca_CA |
dc.description.sponsorShip | Instituto de Salud Carlos III, Ministerio de Economía y Competitividad, España; Grant numbers: PI11/00327, CB06/04/0071; Grant sponsor: Generalitat Valenciana, España; Grant numbers: PROMETEOII/2014/035, GV/2014/118 | ca_CA |
dc.format.extent | 10 p. | ca_CA |
dc.format.mimetype | application/pdf | ca_CA |
dc.language.iso | eng | ca_CA |
dc.publisher | Wiley | ca_CA |
dc.relation.isPartOf | Journal of cellular biochemistry, 2015, vol. 116, no 10 | ca_CA |
dc.rights | © 2015 Wiley Periodicals, Inc. | ca_CA |
dc.rights.uri | http://rightsstatements.org/vocab/InC/1.0/ | * |
dc.subject | Aspirin | ca_CA |
dc.subject | Heat preconditioning | ca_CA |
dc.subject | HSP70 | ca_CA |
dc.subject | Liver regeneration | ca_CA |
dc.title | Heat Stress Induces Extended Plateau of Hsp70 Accumulation – A Possible Cytoprotection Mechanism in Hepatic Cells | ca_CA |
dc.type | info:eu-repo/semantics/article | ca_CA |
dc.identifier.doi | http://dx.doi.org/10.1002/jcb.25187 | |
dc.rights.accessRights | info:eu-repo/semantics/restrictedAccess | ca_CA |
dc.relation.publisherVersion | http://onlinelibrary.wiley.com/doi/10.1002/jcb.25187/full | ca_CA |
dc.type.version | info:eu-repo/semantics/publishedVersion |
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