File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Type II SOCS as a feedback repressor for GH-induced Igf1 expression in carp hepatocytes

TitleType II SOCS as a feedback repressor for GH-induced Igf1 expression in carp hepatocytes
Authors
Issue Date2016
PublisherSociety for Endocrinology. The Journal's web site is located at http://joe.endocrinology-journals.org
Citation
Journal of Endocrinology, 2016, v. 229 n. 2, p. 171-186 How to Cite?
AbstractType II suppressor of cytokine signaling (SOCS) serve as feedback repressors for cytokines and are known to inhibit growth hormone (GH) actions. However, direct evidence for SOCS modulation of GH-induced insulin-like growth factor 1 (Igf1) expression is lacking, and the post-receptor signaling for SOCS expression at the hepatic level is still unclear. To shed light on the comparative aspects of SOCS in GH functions, grass carp was used as a model to study the role of type II SOCS in GH-induced Igf1 expression. Structural identity of type II SOCS, Socs1-3 and cytokine-inducible SH2-containing protein (Cish), was established in grass carp by 5'/3'-RACE, and their expression at both transcript and protein levels were confirmed in the liver by RT-PCR and LC/MS/MS respectively. In carp hepatocytes, GH treatment induced rapid phosphorylation of JAK2, STATs, MAPK, PI3K, and protein kinase B (Akt) with parallel rises in socs1-3 and cish mRNA levels, and these stimulatory effects on type II SOCS were shown to occur before the gradual loss of igf1 gene expression caused by prolonged exposure of GH. Furthermore, GH-induced type II SOCS gene expression could be negated by inhibiting JAK2, STATs, MEK1/2, P38 (MAPK), PI3K, and/or Akt respectively. In CHO cells transfected with carp GH receptor, over-expression of these newly cloned type II SOCS not only suppressed JAK2/STAT5 signaling with GH treatment but also inhibited GH-induced grass carp Igf1 promoter activity. These results, taken together, suggest that type II SOCS could be induced by GH in the carp liver via JAK2/STATs, MAPK, and PI3K/Akt cascades and serve as feedback repressors for GH signaling and induction of igf1 gene expression.
Persistent Identifierhttp://hdl.handle.net/10722/230285
ISSN
2015 Impact Factor: 4.498
2015 SCImago Journal Rankings: 1.910

 

DC FieldValueLanguage
dc.contributor.authorJIANG, X-
dc.contributor.authorHe, M-
dc.contributor.authorMA, A-
dc.contributor.authorWong, AOL-
dc.date.accessioned2016-08-23T14:16:10Z-
dc.date.available2016-08-23T14:16:10Z-
dc.date.issued2016-
dc.identifier.citationJournal of Endocrinology, 2016, v. 229 n. 2, p. 171-186-
dc.identifier.issn0022-0795-
dc.identifier.urihttp://hdl.handle.net/10722/230285-
dc.description.abstractType II suppressor of cytokine signaling (SOCS) serve as feedback repressors for cytokines and are known to inhibit growth hormone (GH) actions. However, direct evidence for SOCS modulation of GH-induced insulin-like growth factor 1 (Igf1) expression is lacking, and the post-receptor signaling for SOCS expression at the hepatic level is still unclear. To shed light on the comparative aspects of SOCS in GH functions, grass carp was used as a model to study the role of type II SOCS in GH-induced Igf1 expression. Structural identity of type II SOCS, Socs1-3 and cytokine-inducible SH2-containing protein (Cish), was established in grass carp by 5'/3'-RACE, and their expression at both transcript and protein levels were confirmed in the liver by RT-PCR and LC/MS/MS respectively. In carp hepatocytes, GH treatment induced rapid phosphorylation of JAK2, STATs, MAPK, PI3K, and protein kinase B (Akt) with parallel rises in socs1-3 and cish mRNA levels, and these stimulatory effects on type II SOCS were shown to occur before the gradual loss of igf1 gene expression caused by prolonged exposure of GH. Furthermore, GH-induced type II SOCS gene expression could be negated by inhibiting JAK2, STATs, MEK1/2, P38 (MAPK), PI3K, and/or Akt respectively. In CHO cells transfected with carp GH receptor, over-expression of these newly cloned type II SOCS not only suppressed JAK2/STAT5 signaling with GH treatment but also inhibited GH-induced grass carp Igf1 promoter activity. These results, taken together, suggest that type II SOCS could be induced by GH in the carp liver via JAK2/STATs, MAPK, and PI3K/Akt cascades and serve as feedback repressors for GH signaling and induction of igf1 gene expression.-
dc.languageeng-
dc.publisherSociety for Endocrinology. The Journal's web site is located at http://joe.endocrinology-journals.org-
dc.relation.ispartofJournal of Endocrinology-
dc.rights'Disclaimer. This is not the definitive version of record of this article. This manuscript has been accepted for publication in [insert name of journal], but the version presented here has not yet been copy edited, formatted or proofed. Consequently, the Society for Endocrinology accepts no responsibility for any errors or omissions it may contain. The definitive version is now freely available at [insert DOI link][insert year of publication] Society for Endocrinology.'-
dc.titleType II SOCS as a feedback repressor for GH-induced Igf1 expression in carp hepatocytes-
dc.typeArticle-
dc.identifier.emailHe, M: hemu@hkucc.hku.hk-
dc.identifier.emailWong, AOL: olwong@hkucc.hku.hk-
dc.identifier.authorityWong, AOL=rp00806-
dc.identifier.doi10.1530/JOE-15-0423-
dc.identifier.pmid27271287-
dc.identifier.hkuros261859-
dc.identifier.hkuros261858-
dc.identifier.volume229-
dc.identifier.issue2-
dc.identifier.spage171-
dc.identifier.epage186-
dc.publisher.placeUnited Kingdom-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats