Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/4066
Title: The influence of dexamethasone on Hsp70 level and association with glucocorticoid receptor in the liver of unstressed and heat stressed rats
Authors: Dundjerski, J.
Vidović, S.
Matić, Gordana 
Issue Date: 2003
Journal: Yugoslav. Med. Biochem.
Series/Report no.: 22;19-26
Abstract: 
The aim of the present study was to examine the influence of dexamethasone on the levels of
heat shock protein Hsp70 and glucocorticoid hormones receptor, as well as on the interaction of these two proteins
in the liver cytosol and nuclei of unstressed and rats exposed to whole body hyperthermic stress. The results,
obtained by quantitative immunoblotting, have shown that dexamethasone provoked a reduction of Hsp70 basal
level and an increase in its stress-induced level in the nuclei, supporting the idea that this hormone may be a factor
included in the regulation of Hsp70 level both under normal and stress conditions. The cytosolic reduction and
nuclear elevation of the glucocorticoid hormones receptor level by dexamethasone were also observed. Coimmunopurification
of Hsp70 and glucocorticoid hormones receptor has revealed that the changes of cytosolic
and nuclear levels of the two examined proteins resulted in the changes of their interaction within the respective
cellular compartments. Thus, 41 °C heat stress, was shown to cause at least two-fold elevation of Hsp70/GR ratio
within the glucocorticoid hormones receptor heterocomplexes both in the presence and in the absence of dexamethasone.
The results support the view that glucocorticoid hormones signaling pathway and heat shock system
are interrelated.
URI: https://biore.bio.bg.ac.rs/handle/123456789/4066
ISSN: 0354-3447
Appears in Collections:Journal Article

Files in This Item:
File Description SizeFormat Existing users please
Dundjerski-JugMedBiohem-2003.pdf124.1 kBAdobe PDF
    Request a copy
Show full item record

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.