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Article: Signaling mechanisms for α2-adrenergic inhibition of PACAP-induced growth hormone secretion and gene expression grass carp pituitary cells

TitleSignaling mechanisms for α2-adrenergic inhibition of PACAP-induced growth hormone secretion and gene expression grass carp pituitary cells
Authors
Issue Date2007
PublisherAmerican Physiological Society. The Journal's web site is located at http://ajpendo.physiology.org/
Citation
American Journal Of Physiology - Endocrinology And Metabolism, 2007, v. 292 n. 6, p. E1750-E1762 How to Cite?
AbstractPituitary adenylate cyclase-activating polypeptide (PACAP) is a potent growth hormone (GH)-releasing factor in lower vertebrates. However, its functional interactions with other GH regulators have not been fully characterized. In fish models, norepinephrine (NE) inhibits GH release at the pituitary cell level, but its effects on GH synthesis have yet to be determined. We examined adrenergic inhibition of PACAP-induced GH secretion and GH gene expression using grass carp pituitary cells as a cell model. Through activation of pituitary α2-adrenoreceptors, NE or the α2- agonist clonidine reduced both basal and PACAP-induced GH release and GH mRNA expression. In carp pituitary cells, clonidine also suppressed cAMP production and intracellular Ca2+ levels and blocked PACAP induction of these two second messenger signals. In GH3 cells transfected with a reporter carrying the grass carp GH promoter, PACAP stimulation increased GH promoter activity, and this stimulatory effect could be abolished by NE treatment. In parallel experiments, clonidine reduced GH primary transcript and GH promoter activity without affecting GH mRNA stability, and these inhibitory actions were mimicked by inhibiting adenylate cyclase (AC), blocking protein kinase A (PKA), removing extracellular Ca2+ in the culture medium, or inactivating L-type voltage-sensitive Ca2+ channels (VSCC). Since our recent studies have shown that PACAP can induce GH secretion in carp pituitary cells through cAMP/PKA- and Ca2+/calmodulin-dependent mechanisms, these results, taken together, suggest that α2-adrenergic stimulation in the carp pituitary may inhibit PACAP-induced GH release and GH gene transcription by blocking the AC/cAMP/PKA pathway and Ca2+ entry through L-type VSCC. Copyright © 2007 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/179007
ISSN
2015 Impact Factor: 3.825
2015 SCImago Journal Rankings: 2.465
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Xen_US
dc.contributor.authorChu, MMSen_US
dc.contributor.authorWong, AOLen_US
dc.date.accessioned2012-12-19T09:51:22Z-
dc.date.available2012-12-19T09:51:22Z-
dc.date.issued2007en_US
dc.identifier.citationAmerican Journal Of Physiology - Endocrinology And Metabolism, 2007, v. 292 n. 6, p. E1750-E1762en_US
dc.identifier.issn0193-1849en_US
dc.identifier.urihttp://hdl.handle.net/10722/179007-
dc.description.abstractPituitary adenylate cyclase-activating polypeptide (PACAP) is a potent growth hormone (GH)-releasing factor in lower vertebrates. However, its functional interactions with other GH regulators have not been fully characterized. In fish models, norepinephrine (NE) inhibits GH release at the pituitary cell level, but its effects on GH synthesis have yet to be determined. We examined adrenergic inhibition of PACAP-induced GH secretion and GH gene expression using grass carp pituitary cells as a cell model. Through activation of pituitary α2-adrenoreceptors, NE or the α2- agonist clonidine reduced both basal and PACAP-induced GH release and GH mRNA expression. In carp pituitary cells, clonidine also suppressed cAMP production and intracellular Ca2+ levels and blocked PACAP induction of these two second messenger signals. In GH3 cells transfected with a reporter carrying the grass carp GH promoter, PACAP stimulation increased GH promoter activity, and this stimulatory effect could be abolished by NE treatment. In parallel experiments, clonidine reduced GH primary transcript and GH promoter activity without affecting GH mRNA stability, and these inhibitory actions were mimicked by inhibiting adenylate cyclase (AC), blocking protein kinase A (PKA), removing extracellular Ca2+ in the culture medium, or inactivating L-type voltage-sensitive Ca2+ channels (VSCC). Since our recent studies have shown that PACAP can induce GH secretion in carp pituitary cells through cAMP/PKA- and Ca2+/calmodulin-dependent mechanisms, these results, taken together, suggest that α2-adrenergic stimulation in the carp pituitary may inhibit PACAP-induced GH release and GH gene transcription by blocking the AC/cAMP/PKA pathway and Ca2+ entry through L-type VSCC. Copyright © 2007 the American Physiological Society.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://ajpendo.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Endocrinology and Metabolismen_US
dc.subject.meshAdenylate Cyclase - Antagonists & Inhibitorsen_US
dc.subject.meshAdrenergic Alpha-Agonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Metabolismen_US
dc.subject.meshCalcium Channels, L-Type - Drug Effectsen_US
dc.subject.meshCarpsen_US
dc.subject.meshCell Lineen_US
dc.subject.meshClonidine - Pharmacologyen_US
dc.subject.meshCyclic Amp - Antagonists & Inhibitors - Biosynthesisen_US
dc.subject.meshCyclic Amp-Dependent Protein Kinases - Antagonists & Inhibitorsen_US
dc.subject.meshGene Expression - Drug Effectsen_US
dc.subject.meshGrowth Hormone - Antagonists & Inhibitors - Genetics - Secretionen_US
dc.subject.meshIntracellular Membranes - Metabolismen_US
dc.subject.meshPituitary Adenylate Cyclase-Activating Polypeptide - Pharmacologyen_US
dc.subject.meshPituitary Gland - Cytology - Metabolism - Secretionen_US
dc.subject.meshPromoter Regions, Genetic - Drug Effectsen_US
dc.subject.meshRna Stability - Drug Effectsen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshSignal Transduction - Physiologyen_US
dc.subject.meshTranscription, Genetic - Drug Effectsen_US
dc.subject.meshTransfectionen_US
dc.titleSignaling mechanisms for α2-adrenergic inhibition of PACAP-induced growth hormone secretion and gene expression grass carp pituitary cellsen_US
dc.typeArticleen_US
dc.identifier.emailWong, AOL: olwong@hkucc.hku.hken_US
dc.identifier.authorityWong, AOL=rp00806en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1152/ajpendo.00001.2007en_US
dc.identifier.pmid17311897-
dc.identifier.scopuseid_2-s2.0-34447552536en_US
dc.identifier.hkuros151099-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34447552536&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume292en_US
dc.identifier.issue6en_US
dc.identifier.spageE1750en_US
dc.identifier.epageE1762en_US
dc.identifier.eissn1522-1555-
dc.identifier.isiWOS:000247939100028-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWang, X=8941883500en_US
dc.identifier.scopusauthoridChu, MMS=8761175900en_US
dc.identifier.scopusauthoridWong, AOL=7403147570en_US
dc.identifier.citeulike3813137-

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