File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Paracrine regulation of growth hormone gene expression by gonadotrophin release in grass carp pituitary cells: Functional implications, molecular mechanisms and signal transduction

TitleParacrine regulation of growth hormone gene expression by gonadotrophin release in grass carp pituitary cells: Functional implications, molecular mechanisms and signal transduction
Authors
Issue Date2005
PublisherSociety for Endocrinology. The Journal's web site is located at http://jme.endocrinology-journals.org/
Citation
Journal Of Molecular Endocrinology, 2005, v. 34 n. 2, p. 415-432 How to Cite?
AbstractGrowth hormone (GH) is known to stimulate luteinizing hormone (LH) release via paracrine interactions between somatotrophs and gonadotrophs. However, it is unclear if LH can exert a reciprocal effect to modulate somatotroph functions. Here we examined the paracrine effects of LH on GH gene expression using grass carp pituitary cells as a cell model. LH receptors were identified in grass carp somatotrophs and their activation by human chorionic gonadotropin (hCG) increased 'steady-state' GH mRNA levels. Removal of endogenous LH by immunoneutralization using LH antiserum inhibited GH release and GH mRNA expression. GH secretagogues, including gonadotrophin releasing hormone (GnRH), pituitary adenylate cyclase-activating polypeptide (PACAP) and apomorphine, were effective in elevating GH mRNA levels but these stimulatory actions were blocked by LH antiserum. In pituitary cells pretreated with actinomycin D, the half-life of GH mRNA was not affected by hCG but was enhanced by LH immunoneutralization. Treatment with LH antiserum also suppressed basal levels of mature GH mRNA and primary transcripts. hCG increased cAMP synthesis in carp pituitary cells and hCG-induced GH mRNA expression was mimicked by forskolin but suppressed by inhibiting adenylate cyclase and protein kinase A. Similarly, the stimulatory actions of hCG and forskolin on GH mRNA expression were blocked by inhibiting Janus kinase 2 (JAK2) and MAP kinase (MAPK), including P42/44 MAPK and P38 MAPK. These results suggest that LH is essential for the maintenance of GH release, GH gene expression, and somatotroph responsiveness to GH-releasing factors. The paracrine actions of LH on GH mRNA expression are mediated by a concurrent increase in GH gene transcription and GH mRNA turnover, probably through JAK2/MAPK coupled to the cAMP-dependent pathway. © 2005 Society for Endocrinology.
Persistent Identifierhttp://hdl.handle.net/10722/178874
ISSN
2015 Impact Factor: 2.947
2015 SCImago Journal Rankings: 1.674
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhou, Hen_US
dc.contributor.authorJiang, Yen_US
dc.contributor.authorKo, WKWen_US
dc.contributor.authorLi, Wen_US
dc.contributor.authorWong, AOLen_US
dc.date.accessioned2012-12-19T09:50:19Z-
dc.date.available2012-12-19T09:50:19Z-
dc.date.issued2005en_US
dc.identifier.citationJournal Of Molecular Endocrinology, 2005, v. 34 n. 2, p. 415-432en_US
dc.identifier.issn0952-5041en_US
dc.identifier.urihttp://hdl.handle.net/10722/178874-
dc.description.abstractGrowth hormone (GH) is known to stimulate luteinizing hormone (LH) release via paracrine interactions between somatotrophs and gonadotrophs. However, it is unclear if LH can exert a reciprocal effect to modulate somatotroph functions. Here we examined the paracrine effects of LH on GH gene expression using grass carp pituitary cells as a cell model. LH receptors were identified in grass carp somatotrophs and their activation by human chorionic gonadotropin (hCG) increased 'steady-state' GH mRNA levels. Removal of endogenous LH by immunoneutralization using LH antiserum inhibited GH release and GH mRNA expression. GH secretagogues, including gonadotrophin releasing hormone (GnRH), pituitary adenylate cyclase-activating polypeptide (PACAP) and apomorphine, were effective in elevating GH mRNA levels but these stimulatory actions were blocked by LH antiserum. In pituitary cells pretreated with actinomycin D, the half-life of GH mRNA was not affected by hCG but was enhanced by LH immunoneutralization. Treatment with LH antiserum also suppressed basal levels of mature GH mRNA and primary transcripts. hCG increased cAMP synthesis in carp pituitary cells and hCG-induced GH mRNA expression was mimicked by forskolin but suppressed by inhibiting adenylate cyclase and protein kinase A. Similarly, the stimulatory actions of hCG and forskolin on GH mRNA expression were blocked by inhibiting Janus kinase 2 (JAK2) and MAP kinase (MAPK), including P42/44 MAPK and P38 MAPK. These results suggest that LH is essential for the maintenance of GH release, GH gene expression, and somatotroph responsiveness to GH-releasing factors. The paracrine actions of LH on GH mRNA expression are mediated by a concurrent increase in GH gene transcription and GH mRNA turnover, probably through JAK2/MAPK coupled to the cAMP-dependent pathway. © 2005 Society for Endocrinology.en_US
dc.languageengen_US
dc.publisherSociety for Endocrinology. The Journal's web site is located at http://jme.endocrinology-journals.org/en_US
dc.relation.ispartofJournal of Molecular Endocrinologyen_US
dc.rightsJournal of Molecular Endocrinology. Copyright © Society for Endocrinology.-
dc.subject.meshAnimalsen_US
dc.subject.meshAntibodies, Monoclonal - Immunologyen_US
dc.subject.meshCarpsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshChorionic Gonadotropin - Metabolismen_US
dc.subject.meshDactinomycin - Metabolismen_US
dc.subject.meshEnzyme Inhibitors - Metabolismen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshGrowth Hormone - Genetics - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshLasersen_US
dc.subject.meshLuteinizing Hormone - Immunology - Metabolismen_US
dc.subject.meshMitogen-Activated Protein Kinases - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshParacrine Communicationen_US
dc.subject.meshPhosphatidylinositol 3-Kinases - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshPituitary Gland - Cytology - Metabolismen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshProtein Synthesis Inhibitors - Metabolismen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshReceptors, Lh - Genetics - Metabolismen_US
dc.subject.meshSignal Transduction - Physiologyen_US
dc.titleParacrine regulation of growth hormone gene expression by gonadotrophin release in grass carp pituitary cells: Functional implications, molecular mechanisms and signal transductionen_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.doi10.1677/jme.1.01629en_US
dc.identifier.pmid15821107-
dc.identifier.scopuseid_2-s2.0-17844377065en_US
dc.identifier.hkuros101436-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-17844377065&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume34en_US
dc.identifier.issue2en_US
dc.identifier.spage415en_US
dc.identifier.epage432en_US
dc.identifier.isiWOS:000228583800012-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridZhou, H=7404742310en_US
dc.identifier.scopusauthoridJiang, Y=15061459000en_US
dc.identifier.scopusauthoridKo, WKW=7202286890en_US
dc.identifier.scopusauthoridLi, W=36062301700en_US
dc.identifier.scopusauthoridWong, AOL=7403147570en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats