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Article: Gene expression of the receptor for growth-hormone-releasing hormone is physiologically regulated by glucocorticoids and estrogen

TitleGene expression of the receptor for growth-hormone-releasing hormone is physiologically regulated by glucocorticoids and estrogen
Authors
KeywordsAdrenal steroids
Adrenalectomy
Castration
Gene expression
Gonadal steroids
Growth hormone
Growth hormone releasing hormone
Growth hormone-releasing hormone receptor
Issue Date1996
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEN
Citation
Neuroendocrinology, 1996, v. 63 n. 6, p. 475-480 How to Cite?
AbstractWe investigated the effects of glucocorticoids and estrogen on the gene expression of growth hormone (GH) and the receptor for growth-hormone-releasing hormone (GHRH) by measuring the mRNA levels of GH and GHRH receptor in pituitary tissues of Sprague-Dawley rats using Northern blot hybridization and specific cDNA probes. Male rats, 6 weeks of age, were either adrenal ectomized (or sham-operated) or treated with varying doses of dexamethasone (40, 200, 500 or 1,000 μg/kg/day, i.p.) for 3 days. Female rats, 4 weeks of age were oophorectomized or sham-operated, and treated with 17β-estradiol benzoate 25 μg/kg/day (or vehicle) s.c. for 5 days starting 10 days after oophorectomy. Adrenalectomy was associated with a reduction in weight gain and decreased GHRH receptor mRNA levels (p < 0.05 and p < 0.0001 versus sham-operated, respectively). Dexamethasone treatment, however, was associated with a dose-dependent reduction in weight gain (p < 0.0001) but dose-dependent increases in GHRH receptor mRNA and GH mRNA levels (p < 0.0001 and p < 0.05, respectively). In the female rats, weight gain was increased by oophorectomy (p < 0.005 vs. sham-operated) and decreased by estrogen treatment (p < 0.05 vs. vehicle-treated). Pituitary GHRH receptor mRNA levels were also increased by oophorectomy (p < 0.05) and decreased by estrogen (p < 0.005). GH mRNA levels were unchanged by oophorectomy but decreased after estrogen treatment (p < 0.05). In conclusion, our findings suggest that endogenous glucocorticoids and estrogen are physiological regulators of pituitary GHRH receptor gene expression. Glucocorticoids and estrogen also regulate GH secretion via effects on GH gene expression. Changes in GHRH receptor and GH mRNA levels cannot explain the growth retardation in dexamethasone-treated rats.
Persistent Identifierhttp://hdl.handle.net/10722/148057
ISSN
2015 Impact Factor: 2.583
2015 SCImago Journal Rankings: 1.479
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorLee, MFen_HK
dc.contributor.authorTam, SPen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.date.accessioned2012-05-29T06:10:37Z-
dc.date.available2012-05-29T06:10:37Z-
dc.date.issued1996en_HK
dc.identifier.citationNeuroendocrinology, 1996, v. 63 n. 6, p. 475-480en_HK
dc.identifier.issn0028-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148057-
dc.description.abstractWe investigated the effects of glucocorticoids and estrogen on the gene expression of growth hormone (GH) and the receptor for growth-hormone-releasing hormone (GHRH) by measuring the mRNA levels of GH and GHRH receptor in pituitary tissues of Sprague-Dawley rats using Northern blot hybridization and specific cDNA probes. Male rats, 6 weeks of age, were either adrenal ectomized (or sham-operated) or treated with varying doses of dexamethasone (40, 200, 500 or 1,000 μg/kg/day, i.p.) for 3 days. Female rats, 4 weeks of age were oophorectomized or sham-operated, and treated with 17β-estradiol benzoate 25 μg/kg/day (or vehicle) s.c. for 5 days starting 10 days after oophorectomy. Adrenalectomy was associated with a reduction in weight gain and decreased GHRH receptor mRNA levels (p < 0.05 and p < 0.0001 versus sham-operated, respectively). Dexamethasone treatment, however, was associated with a dose-dependent reduction in weight gain (p < 0.0001) but dose-dependent increases in GHRH receptor mRNA and GH mRNA levels (p < 0.0001 and p < 0.05, respectively). In the female rats, weight gain was increased by oophorectomy (p < 0.005 vs. sham-operated) and decreased by estrogen treatment (p < 0.05 vs. vehicle-treated). Pituitary GHRH receptor mRNA levels were also increased by oophorectomy (p < 0.05) and decreased by estrogen (p < 0.005). GH mRNA levels were unchanged by oophorectomy but decreased after estrogen treatment (p < 0.05). In conclusion, our findings suggest that endogenous glucocorticoids and estrogen are physiological regulators of pituitary GHRH receptor gene expression. Glucocorticoids and estrogen also regulate GH secretion via effects on GH gene expression. Changes in GHRH receptor and GH mRNA levels cannot explain the growth retardation in dexamethasone-treated rats.en_HK
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NENen_HK
dc.relation.ispartofNeuroendocrinologyen_HK
dc.rightsNeuroendocrinology. Copyright © S Karger AG.-
dc.subjectAdrenal steroidsen_HK
dc.subjectAdrenalectomyen_HK
dc.subjectCastrationen_HK
dc.subjectGene expressionen_HK
dc.subjectGonadal steroidsen_HK
dc.subjectGrowth hormoneen_HK
dc.subjectGrowth hormone releasing hormoneen_HK
dc.subjectGrowth hormone-releasing hormone receptoren_HK
dc.subject.meshAnimalsen_US
dc.subject.meshBlotting, Northernen_US
dc.subject.meshDexamethasone - Pharmacologyen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEstrogens - Pharmacologyen_US
dc.subject.meshGene Expression - Drug Effectsen_US
dc.subject.meshGlucocorticoids - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, Neuropeptide - Drug Effectsen_US
dc.subject.meshReceptors, Pituitary Hormone-Regulating Hormone - Drug Effectsen_US
dc.titleGene expression of the receptor for growth-hormone-releasing hormone is physiologically regulated by glucocorticoids and estrogenen_HK
dc.typeArticleen_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailSrivastava, G: gopesh@pathology.hku.hken_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1159/000127075-
dc.identifier.pmid8793888-
dc.identifier.scopuseid_2-s2.0-0029886191en_HK
dc.identifier.hkuros14326-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029886191&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume63en_HK
dc.identifier.issue6en_HK
dc.identifier.spage475en_HK
dc.identifier.epage480en_HK
dc.identifier.isiWOS:A1996UR45900001-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridLee, MF=8277448500en_HK
dc.identifier.scopusauthoridTam, SP=7202036931en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK
dc.customcontrol.immutablesml 130621-

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