File Download
There are no files associated with this item.
Links for fulltext
(May Require Subscription)
- Publisher Website: 10.1152/ajpendo.00001.2007
- Scopus: eid_2-s2.0-34447552536
- PMID: 17311897
- WOS: WOS:000247939100028
- Find via
Supplementary
-
Bookmarks:
- CiteULike: 1
- Citations:
- Appears in Collections:
Article: Signaling mechanisms for α2-adrenergic inhibition of PACAP-induced growth hormone secretion and gene expression grass carp pituitary cells
Title | Signaling mechanisms for α2-adrenergic inhibition of PACAP-induced growth hormone secretion and gene expression grass carp pituitary cells |
---|---|
Authors | |
Keywords | Growth hormone Norepinephrine Pituitary adenylate cyclase-activating polypeptide Signal transduction |
Issue Date | 2007 |
Publisher | American 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? |
Abstract | Pituitary 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 Identifier | http://hdl.handle.net/10722/179007 |
ISSN | 2023 Impact Factor: 4.2 2023 SCImago Journal Rankings: 1.479 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Wang, X | en_US |
dc.contributor.author | Chu, MMS | en_US |
dc.contributor.author | Wong, AOL | en_US |
dc.date.accessioned | 2012-12-19T09:51:22Z | - |
dc.date.available | 2012-12-19T09:51:22Z | - |
dc.date.issued | 2007 | en_US |
dc.identifier.citation | American Journal Of Physiology - Endocrinology And Metabolism, 2007, v. 292 n. 6, p. E1750-E1762 | en_US |
dc.identifier.issn | 0193-1849 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/179007 | - |
dc.description.abstract | Pituitary 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.language | eng | en_US |
dc.publisher | American Physiological Society. The Journal's web site is located at http://ajpendo.physiology.org/ | en_US |
dc.relation.ispartof | American Journal of Physiology - Endocrinology and Metabolism | en_US |
dc.subject | Growth hormone | - |
dc.subject | Norepinephrine | - |
dc.subject | Pituitary adenylate cyclase-activating polypeptide | - |
dc.subject | Signal transduction | - |
dc.subject.mesh | Adenylate Cyclase - Antagonists & Inhibitors | en_US |
dc.subject.mesh | Adrenergic Alpha-Agonists - Pharmacology | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Calcium - Metabolism | en_US |
dc.subject.mesh | Calcium Channels, L-Type - Drug Effects | en_US |
dc.subject.mesh | Carps | en_US |
dc.subject.mesh | Cell Line | en_US |
dc.subject.mesh | Clonidine - Pharmacology | en_US |
dc.subject.mesh | Cyclic Amp - Antagonists & Inhibitors - Biosynthesis | en_US |
dc.subject.mesh | Cyclic Amp-Dependent Protein Kinases - Antagonists & Inhibitors | en_US |
dc.subject.mesh | Gene Expression - Drug Effects | en_US |
dc.subject.mesh | Growth Hormone - Antagonists & Inhibitors - Genetics - Secretion | en_US |
dc.subject.mesh | Intracellular Membranes - Metabolism | en_US |
dc.subject.mesh | Pituitary Adenylate Cyclase-Activating Polypeptide - Pharmacology | en_US |
dc.subject.mesh | Pituitary Gland - Cytology - Metabolism - Secretion | en_US |
dc.subject.mesh | Promoter Regions, Genetic - Drug Effects | en_US |
dc.subject.mesh | Rna Stability - Drug Effects | en_US |
dc.subject.mesh | Rna, Messenger - Metabolism | en_US |
dc.subject.mesh | Signal Transduction - Physiology | en_US |
dc.subject.mesh | Transcription, Genetic - Drug Effects | en_US |
dc.subject.mesh | Transfection | en_US |
dc.title | Signaling mechanisms for α2-adrenergic inhibition of PACAP-induced growth hormone secretion and gene expression grass carp pituitary cells | en_US |
dc.type | Article | en_US |
dc.identifier.email | Wong, AOL: olwong@hkucc.hku.hk | en_US |
dc.identifier.authority | Wong, AOL=rp00806 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1152/ajpendo.00001.2007 | en_US |
dc.identifier.pmid | 17311897 | - |
dc.identifier.scopus | eid_2-s2.0-34447552536 | en_US |
dc.identifier.hkuros | 151099 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-34447552536&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 292 | en_US |
dc.identifier.issue | 6 | en_US |
dc.identifier.spage | E1750 | en_US |
dc.identifier.epage | E1762 | en_US |
dc.identifier.eissn | 1522-1555 | - |
dc.identifier.isi | WOS:000247939100028 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Wang, X=8941883500 | en_US |
dc.identifier.scopusauthorid | Chu, MMS=8761175900 | en_US |
dc.identifier.scopusauthorid | Wong, AOL=7403147570 | en_US |
dc.identifier.citeulike | 3813137 | - |
dc.identifier.issnl | 0193-1849 | - |