COLD-INDUCED HEAT-SHOCK PROTEIN EXPRESSION IN RAT AORTA AND BROWN ADIPOSE-TISSUE

Citation
Jm. Matz et al., COLD-INDUCED HEAT-SHOCK PROTEIN EXPRESSION IN RAT AORTA AND BROWN ADIPOSE-TISSUE, Physiology & behavior, 60(5), 1996, pp. 1369-1374
Citations number
32
Categorie Soggetti
Psychology, Biological","Behavioral Sciences",Physiology
Journal title
ISSN journal
00319384
Volume
60
Issue
5
Year of publication
1996
Pages
1369 - 1374
Database
ISI
SICI code
0031-9384(1996)60:5<1369:CHPEIR>2.0.ZU;2-K
Abstract
Recent reports indicate that Heat Shock Proteins (HSPs) are induced in mammalian tissues as part of a homeostatic response to environmental stressors. Administration of sympathomimetic drugs and neuroendocrine stress hormones has been shown to evoke an HSP response in unstressed animals indicating that cell signaling events exists that couple speci fic neurotransmitter/hormone-receptor interactions with HSP expression in mammalian tissues. Herein, we demonstrate that exposure of rats to a cold ambient temperature (6 degrees C) results in increased express ion of constitutive and inducible members of the HSP70 gene family in association with increased expression of the mitochondrial uncoupling protein in brown adipose tissue (BAT). Increased HSP70 expression was not restricted to BAT because HSP70 was also induced in the aorta. Thi s cord-induced HSP response is characterized by a transient increase i n HSP70 protein and mRNA in both tissues during continued exposure. Ga nglionic blockade prevented cold-induced HSP70 expression in BAT and a orta, indicating that sympathetic activity is requisite to this respon se. Administration of the alpha(1)-adrenergic receptor antagonist, pra zosin, also blocked expression, further delineating possible signaling mechanisms mediating this response. Apparently, cells in some mammali an tissues have adopted unique cellular regulatory mechanisms to suppo rt HSP induction that have been incorporated into the physiological re sponse of the entire organism to an environmental stressor. Copyright (C) 1996 Elsevier Science Inc.