Sex differences in the regulation of heat shock protein 70 kDa and 90 kDa in the rat ventromedial hypothalamus by estrogen

Olazábal, U.E.; Pfaff, Donald W.; Mobbs, Charles V.

doi:10.1016/0006-8993(92)91563-t

Cited by 33 publications

(23 citation statements)

References 24 publications

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“…This result is consistent with previous reports based on western blot analysis 19,20. Hsp90 chaperones are associated with multiple functions including the regulation of exocytosis and endocytosis 21,22.…”

Section: Discussionsupporting

confidence: 93%

Estrogen Regulation of Proteins in the Rat Ventromedial Nucleus of the Hypothalamus

Callegari

Telefont

et al. 2008

J. Proteome Res.

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The effects of estradiol (E 2 ) on the expression of proteins in the pars lateralis of the ventromedial nucleus of the hypothalamus (VMNpl) in ovariectomized rats was studied using 2-dimensional gel electrophoresis followed by RPLC-nanoESI-MS/MS. E 2 treatment resulted in the up-regulation of 29 identified proteins. Many of these proteins are implicated in the promotion of neuronal plasticity and signaling.

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Section: Discussionsupporting

confidence: 93%

Estrogen Regulation of Proteins in the Rat Ventromedial Nucleus of the Hypothalamus

Callegari

Telefont

et al. 2008

J. Proteome Res.

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“…14.1a ). This fi nding is consistent with previous studies (Olazábal et al 1992a ;Thorp et al 2007 ) and supports the notion that there are no sex differences in the baseline levels of Hsp70 in the hippocampus of female and male rats. The low level of Hsp70 observed in the hippocampus of control animals is also similar to that seen in other studies done exclusively with male rats (Currie and White 1983 ;David et al 1994 ;Armstrong et al 1996 ;Krueger et al 1999 ).…”

Section: Hsp70 and Hsp27 Expression In The Hippocampi Of Control Ratssupporting

confidence: 93%

Neurodegenerative Diseases, Sex Differences and the 27 kDa Heat Shock Protein in the Nervous System

Rioux

Murphy

Esser

et al. 2015

Heat Shock Proteins

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There are sex differences in degenerative disease prevalence in humans. Most models of degenerative disease use male animals. Examining female and male responses to stress may give insight into disease prevalence. Heat shock proteins are chaperones linked to damaged proteins in degenerative diseases and may be expressed differentially in females and males. We have characterized the induced expression of Hsp27 and Hsp70 in the brain and the heart of female and male rats. Rats were heat shocked, brains were removed 24 h after, and western analyses were done to quantify the expression of these proteins. Immunofl uorescence was used to localize Hsp70 and Hsp27 in the hippocampus. Overall, male rats have signifi cantly greater induced expression of both Hsp27 and Hsp70 in the brain. In the hippocampus, Hsp27 was localized in astrocytes, and Hsp70 was localized in blood vessels and microglia, following heat shock. Therefore, the difference in expression of heat shock proteins seen in the brain of male and female rats following heat shock suggests that sex hormones may have an impact on degenerative disease prevalence.

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“…In this regard, various chaperones, including BAG1 and Hsp70, interact with and modulate the activity of steroid receptors (40). Recent studies also demonstrate gender differences in both basal and inducible levels of various chaperones (41)(42)(43)(44) and that such gender-specific differences can be modulated by sex steroids (45,46). For example, estradiol increases chaperone expression in brain tissue (47), whereas testosterone inhibits the up-regulation of Hsp70 and Hsp90 in brain tissue following ischemia/reperfusion in rats (48).…”

Section: Discussionmentioning

confidence: 99%

Sex-dependent Effect of BAG1 in Ameliorating Motor Deficits of Huntington Disease Transgenic Mice

Orr

Huang

Roberts

et al. 2008

Journal of Biological Chemistry

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The pathogenesis of Huntington disease (HD) is attributed to the misfolding of huntingtin (htt) caused by an expanded polyglutamine (polyQ) domain. Considerable effort has been devoted to identifying molecules that can prevent or reduce htt misfolding and the associated neuropathology. Although overexpression of chaperones is known to reduce htt cytotoxicity in cellular models, only modest protection is seen with Hsp70 overexpression in HD mouse models. Because the activity of Hsp70 is modulated by co-chaperones, an interesting issue is whether the in vivo effects of chaperones on polyQ protein toxicity are dependent on other modulators. In the present study, we focused on BAG1, a co-chaperone that interacts with Hsp70 and regulates its activity. Of htt mice expressing the N171-82Q mutant, we found that male N171-82Q mice show a greater deficit in rotarod performance than female N171-82Q mice. This sex-dependent motor deficit was improved by crossing N171-82Q mice with transgenic mice overexpressing BAG1 in neurons. Transgenic BAG1 also reduces the levels of mutant htt in synaptosomal fraction of male HD mice. Overexpression of BAG1 augmented the effects of Hsp70 by reducing aggregation of mutant htt in cultured cells and improving neurite outgrowth in htt-transfected PC12 cells. These findings suggest that the effects of chaperones on HD pathology are influenced by both their modulators and sex-dependent factors. Huntington disease (HD)2 is an inherited neurodegenerative disease caused by a polyglutamine (polyQ) repeat expansion near the N terminus of the protein huntingtin (htt) (HD collaborative research group (49). Patients with HD suffer an array of cognitive, psychiatric, and motor disorders before death, which typically occurs 10 -20 years after onset of symptoms. Pathological hallmarks of this disease include selective neuronal loss and htt inclusions or aggregates that are formed in neuronal nuclei and processes (1, 2). Several genetic mouse models of HD have been developed, and they recapitulate various aspects of the disease observed in patients, including age-dependent inclusion formation and behavioral abnormalities (3). Of these mouse models, the transgenic N171-82Q model, which was generated by using the mouse prion promoter to drive neuronal expression of N-terminal mutant htt, exhibits progressive inclusion formation, motor deficits, weight loss, and shortened life-span (4). The well characterized phenotypes of HD transgenic mice have proven valuable for evaluating potential therapeutics.Misfolding of mutant htt is thought to contribute to abnormal protein-protein interactions, inclusion formation, and neuronal death. Currently, no treatment exists for those afflicted with HD, although considerable attention has been given to molecules that might alleviate the burden of misfolded htt. The major cytosolic chaperones of the Hsp40 and Hsp70 families act in concert to recognize misfolded proteins and refold them. Hsp70 family members interact with mutant N-terminal htt fragments and localize to incl...

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Sex differences in the regulation of heat shock protein 70 kDa and 90 kDa in the rat ventromedial hypothalamus by estrogen

Cited by 33 publications

References 24 publications

Estrogen Regulation of Proteins in the Rat Ventromedial Nucleus of the Hypothalamus

Estrogen Regulation of Proteins in the Rat Ventromedial Nucleus of the Hypothalamus

Neurodegenerative Diseases, Sex Differences and the 27 kDa Heat Shock Protein in the Nervous System

Sex-dependent Effect of BAG1 in Ameliorating Motor Deficits of Huntington Disease Transgenic Mice

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