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Article: Regulation of growth hormone release in common carp pituitary cells by pituitary adenylate cyclase-activating polypeptide: Signal transduction involves cAMP- and calcium-dependent mechanisms

TitleRegulation of growth hormone release in common carp pituitary cells by pituitary adenylate cyclase-activating polypeptide: Signal transduction involves cAMP- and calcium-dependent mechanisms
Authors
KeywordsCalcium
Cyclic AMP
Fishes
Growth hormone
Pituitary adenylate cyclase activating polypeptide
Issue Date2002
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEN
Citation
Neuroendocrinology, 2002, v. 76 n. 5, p. 325-338 How to Cite?
AbstractPituitary adenylate cyclase-activating polypeptide (PACAP) is a member of the glucagon/secretin peptide family and its molecular structure is highly conserved among vertebrates. In this study, the role of PACAP in regulating growth hormone (GH) secretion in fish was examined in vitro using common carp pituitary cells under column perifusion. A dose-dependent increase in GH release was observed after exposing pituitary cells to increasing doses of ovine PACAP38 (oPACAP38) and PACAP27 (oPACAP27), but not vasoactive intestinal polypeptide (VIP). A lack of GH response to VIP stimulation is consistent with the pharmacological properties of PAC-1 receptors, suggesting that this receptor subtype may be involved in PACAP-induced GH secretion in carp species. Although the maximal GH responses induced by oPACAP38 and oPACAP27 were similar, the minimal effective dose and ED50 value for oPACAP38 were significantly lower than that for oPACAP27. These results may indicate that common carp PAC-1 receptors are more sensitive to stimulation by oPACAP38 than by oPACAP27. In parallel studies, oPACAP38 and oPACAP27 were also effective in increasing cAMP release, cellular cAMP content, total cAMP production, and intracellular Ca 2+ ([Ca 2+] i) levels in common carp pituitary cells. Besides, the rise in [Ca 2+] i induced by oPACAP38 was blocked by removing extracellular Ca 2+([Ca 2+] e) or by treatment with nifedipine, an inhibitor of voltage-sensitive Ca 2+ channels (VSCC). The dose dependence of PACAP-stimulated GH release in common carp pituitary cells was mimicked by activating adenylate cyclase using forskolin, inhibiting cAMP degradation using IBMX, increasing functional levels of intracellular cAMP using CPT-cAMP, or inducing [Ca 2+] e entry using the Ca 2+ ionophore A23187. In contrast, the GH-releasing effect of oPACAP38 was suppressed by treatment with the adenylate cyclase inhibitor MDL12330A, protein kinase A inhibitor H89, and VSCC blocker nifedipine, or by perifusion with a Ca 2+-free culture medium. These results, as a whole, suggest that PACAP functions as a GH-releasing factor in common carp by activating pituitary receptors resembling mammalian PAC-1 receptors. Apparently, the GH-releasing action of PACAP is mediated through the adenylate cyclase/cAMP/protein kinase A pathway and [Ca 2+] e influx through VSCC. Copyright © 2002 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/84770
ISSN
2015 Impact Factor: 2.583
2015 SCImago Journal Rankings: 1.479
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXiao, Den_HK
dc.contributor.authorChu, MMSen_HK
dc.contributor.authorLee, EKYen_HK
dc.contributor.authorLin, HRen_HK
dc.contributor.authorWong, AOLen_HK
dc.date.accessioned2010-09-06T08:56:55Z-
dc.date.available2010-09-06T08:56:55Z-
dc.date.issued2002en_HK
dc.identifier.citationNeuroendocrinology, 2002, v. 76 n. 5, p. 325-338en_HK
dc.identifier.issn0028-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84770-
dc.description.abstractPituitary adenylate cyclase-activating polypeptide (PACAP) is a member of the glucagon/secretin peptide family and its molecular structure is highly conserved among vertebrates. In this study, the role of PACAP in regulating growth hormone (GH) secretion in fish was examined in vitro using common carp pituitary cells under column perifusion. A dose-dependent increase in GH release was observed after exposing pituitary cells to increasing doses of ovine PACAP38 (oPACAP38) and PACAP27 (oPACAP27), but not vasoactive intestinal polypeptide (VIP). A lack of GH response to VIP stimulation is consistent with the pharmacological properties of PAC-1 receptors, suggesting that this receptor subtype may be involved in PACAP-induced GH secretion in carp species. Although the maximal GH responses induced by oPACAP38 and oPACAP27 were similar, the minimal effective dose and ED50 value for oPACAP38 were significantly lower than that for oPACAP27. These results may indicate that common carp PAC-1 receptors are more sensitive to stimulation by oPACAP38 than by oPACAP27. In parallel studies, oPACAP38 and oPACAP27 were also effective in increasing cAMP release, cellular cAMP content, total cAMP production, and intracellular Ca 2+ ([Ca 2+] i) levels in common carp pituitary cells. Besides, the rise in [Ca 2+] i induced by oPACAP38 was blocked by removing extracellular Ca 2+([Ca 2+] e) or by treatment with nifedipine, an inhibitor of voltage-sensitive Ca 2+ channels (VSCC). The dose dependence of PACAP-stimulated GH release in common carp pituitary cells was mimicked by activating adenylate cyclase using forskolin, inhibiting cAMP degradation using IBMX, increasing functional levels of intracellular cAMP using CPT-cAMP, or inducing [Ca 2+] e entry using the Ca 2+ ionophore A23187. In contrast, the GH-releasing effect of oPACAP38 was suppressed by treatment with the adenylate cyclase inhibitor MDL12330A, protein kinase A inhibitor H89, and VSCC blocker nifedipine, or by perifusion with a Ca 2+-free culture medium. These results, as a whole, suggest that PACAP functions as a GH-releasing factor in common carp by activating pituitary receptors resembling mammalian PAC-1 receptors. Apparently, the GH-releasing action of PACAP is mediated through the adenylate cyclase/cAMP/protein kinase A pathway and [Ca 2+] e influx through VSCC. Copyright © 2002 S. Karger AG, Basel.en_HK
dc.languageengen_HK
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.en_HK
dc.subjectCalciumen_HK
dc.subjectCyclic AMPen_HK
dc.subjectFishesen_HK
dc.subjectGrowth hormoneen_HK
dc.subjectPituitary adenylate cyclase activating polypeptideen_HK
dc.titleRegulation of growth hormone release in common carp pituitary cells by pituitary adenylate cyclase-activating polypeptide: Signal transduction involves cAMP- and calcium-dependent mechanismsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0028-3835&volume=76&spage=325&epage=338&date=2002&atitle=Regulation+of+Growth+Hormone+Release+in+Common+Carp+Pituitary+Cells+by+Pituitary+Adenylate+Cyclase-Activating+Polypeptide:+Signal+Transduction+Involves+cAMP-+and+Calcium-Dependent+Mechanismsen_HK
dc.identifier.emailWong, AOL: olwong@hkucc.hku.hken_HK
dc.identifier.authorityWong, AOL=rp00806en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000066627en_HK
dc.identifier.pmid12457043-
dc.identifier.scopuseid_2-s2.0-0036442842en_HK
dc.identifier.hkuros75620en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036442842&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume76en_HK
dc.identifier.issue5en_HK
dc.identifier.spage325en_HK
dc.identifier.epage338en_HK
dc.identifier.isiWOS:000179849600007-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridXiao, D=45561966600en_HK
dc.identifier.scopusauthoridChu, MMS=8761175900en_HK
dc.identifier.scopusauthoridLee, EKY=7406968652en_HK
dc.identifier.scopusauthoridLin, HR=7405571313en_HK
dc.identifier.scopusauthoridWong, AOL=7403147570en_HK

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