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Article: Insulin-like growth factor as a novel stimulator for somatolactin secretion and synthesis in carp pituitary cells via activation of MAPK cascades

TitleInsulin-like growth factor as a novel stimulator for somatolactin secretion and synthesis in carp pituitary cells via activation of MAPK cascades
Authors
Issue Date2011
PublisherAmerican Physiological Society. The Journal's web site is located at http://ajpendo.physiology.org/
Citation
American Journal Of Physiology - Endocrinology And Metabolism, 2011, v. 301 n. 6, p. E1208-E1219 How to Cite?
AbstractSomatolactin (SL), a member of the growth hormone/prolactin family, is a pituitary hormone unique to fish models. Although SL is known to have diverse functions in fish, the mechanisms regulating its secretion and synthesis have not been fully characterized. Using grass carp pituitary cells as a model, here we examined the role of insulin-like growth factor (IGF) in SL regulation at the pituitary level. As a first step, the antisera for the two SL isoforms expressed in the carp pituitary, SLα and SLβ, were produced, and their specificity was confirmed by antiserum preabsorption and immunohistochemical staining in the carp pituitary. Western blot using these antisera revealed that grass carp SLα and SLβ could be N-linked glycosylated and their basal secretion and cell content in carp pituitary cells could be elevated by IGF-I and -II treatment. These stimulatory effects occurred with parallel rises in SLα and SLβ mRNA levels, and these SL gene expression responses were not mimicked by insulin but blocked by IGF-I receptor inactivation. In carp pituitary cells, IGF-I and -II could induce rapid phosphorylation of IGF-I receptor, MEK1/2, ERK1/2, MKK3/6, and p38 MAPK; and SLα and SLβ secretion, protein production, and mRNA expression caused by IGF-I and -II stimulation were negated by inactivating MEK1/2 and p38 MAPK. Parallel inhibition of PI3K and Akt, however, were not effective in these regards. These results, taken together, provide evidence that IGF can upregulate SL secretion and synthesis at the pituitary level via stimulation of MAPK- but not PI3K/Akt-dependent pathways. © 2011 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/179264
ISSN
2015 Impact Factor: 3.825
2015 SCImago Journal Rankings: 2.465
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJiang, Qen_US
dc.contributor.authorKo, WKWen_US
dc.contributor.authorWong, AOLen_US
dc.date.accessioned2012-12-19T09:53:28Z-
dc.date.available2012-12-19T09:53:28Z-
dc.date.issued2011en_US
dc.identifier.citationAmerican Journal Of Physiology - Endocrinology And Metabolism, 2011, v. 301 n. 6, p. E1208-E1219en_US
dc.identifier.issn0193-1849en_US
dc.identifier.urihttp://hdl.handle.net/10722/179264-
dc.description.abstractSomatolactin (SL), a member of the growth hormone/prolactin family, is a pituitary hormone unique to fish models. Although SL is known to have diverse functions in fish, the mechanisms regulating its secretion and synthesis have not been fully characterized. Using grass carp pituitary cells as a model, here we examined the role of insulin-like growth factor (IGF) in SL regulation at the pituitary level. As a first step, the antisera for the two SL isoforms expressed in the carp pituitary, SLα and SLβ, were produced, and their specificity was confirmed by antiserum preabsorption and immunohistochemical staining in the carp pituitary. Western blot using these antisera revealed that grass carp SLα and SLβ could be N-linked glycosylated and their basal secretion and cell content in carp pituitary cells could be elevated by IGF-I and -II treatment. These stimulatory effects occurred with parallel rises in SLα and SLβ mRNA levels, and these SL gene expression responses were not mimicked by insulin but blocked by IGF-I receptor inactivation. In carp pituitary cells, IGF-I and -II could induce rapid phosphorylation of IGF-I receptor, MEK1/2, ERK1/2, MKK3/6, and p38 MAPK; and SLα and SLβ secretion, protein production, and mRNA expression caused by IGF-I and -II stimulation were negated by inactivating MEK1/2 and p38 MAPK. Parallel inhibition of PI3K and Akt, however, were not effective in these regards. These results, taken together, provide evidence that IGF can upregulate SL secretion and synthesis at the pituitary level via stimulation of MAPK- but not PI3K/Akt-dependent pathways. © 2011 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.meshAnimalsen_US
dc.subject.meshCarps - Metabolismen_US
dc.subject.meshEnzyme Activation - Drug Effects - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFish Proteins - Biosynthesis - Genetics - Secretionen_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshGlycoproteins - Biosynthesis - Genetics - Secretionen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshInsulin-Like Growth Factor I - Pharmacology - Physiologyen_US
dc.subject.meshMap Kinase Signaling System - Drug Effects - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshPituitary Gland - Cytology - Drug Effects - Metabolismen_US
dc.subject.meshPituitary Hormones - Biosynthesis - Genetics - Secretionen_US
dc.subject.meshProtein Kinase Inhibitors - Pharmacologyen_US
dc.subject.meshSignal Transduction - Drug Effects - Physiologyen_US
dc.subject.meshStimulation, Chemicalen_US
dc.subject.meshUp-Regulation - Drug Effectsen_US
dc.titleInsulin-like growth factor as a novel stimulator for somatolactin secretion and synthesis in carp pituitary cells via activation of MAPK cascadesen_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.00347.2011en_US
dc.identifier.pmid21862722-
dc.identifier.scopuseid_2-s2.0-82355164863en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-82355164863&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume301en_US
dc.identifier.issue6en_US
dc.identifier.spageE1208en_US
dc.identifier.epageE1219en_US
dc.identifier.eissn1522-1555-
dc.identifier.isiWOS:000298141100018-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridJiang, Q=35484035000en_US
dc.identifier.scopusauthoridKo, WKW=7202286890en_US
dc.identifier.scopusauthoridWong, AOL=7403147570en_US

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