Growth hormone stimulates hepatic expression of bovine growth hormone receptor messenger ribonucleic acid through signal transducer and activator of transcription 5 activation of a major growth hormone receptor gene promoter

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dc.contributor.authorJiang, Honglinen
dc.contributor.authorWang, Yingen
dc.contributor.authorWu, Miaozongen
dc.contributor.authorGu, Zhiliangen
dc.contributor.authorFrank, Stuart J.en
dc.contributor.authorTorres-Diaz, Robertoen
dc.contributor.departmentAnimal and Poultry Sciencesen
dc.contributor.departmentLarge Animal Clinical Sciencesen
dc.date.accessed2014-07-07en
dc.date.accessioned2014-07-08T13:02:17Zen
dc.date.available2014-07-08T13:02:17Zen
dc.date.issued2007-07en
dc.description.abstractThe objective of this study was to determine whether and how GH regulates hepatic expression of GH receptor (GHR) mRNA in cattle. Ribonuclease protection assays revealed that injection of GH in a slow-release formula increased both hepatic GHR and IGF-I mRNAs 1 wk after the injection. The increases in GHR and IGF-I mRNAs were highly correlated. Western blot analysis showed that the injection also increased liver GHR protein level. In cattle and other mammals, hepatic GHR mRNA is expressed as variants that differ in the 5'-untranslated region due to the use of different promoters in transcription and/or alternative splicing. We found that GH increased the expression of the liver-specific GHR mRNA variant GHR1A without affecting the other two major GHR mRNA variants in the bovine liver, GHR1B and GHR1C. In transient transfection analyses, GH could robustly activate reporter gene expression from a 2.7-kb GHR1A promoter, suggesting that GH augmentation of GHR1A mRNA expression in the liver is at least partially mediated at the transcriptional level. Additional transfection analyses of serially 5'-truncated fragments of this promoter narrowed the GH-responsive sequence element down to a 210-bp region that contained a putative signal transducer and activator of transcription 5 (STAT5) binding site. EMSAs demonstrated that this putative STAT5 binding site was able to bind to STAT5b protein. In cotransfection assays, deletion of this putative STAT5 binding site abolished most of the GH response of the GHR1A promoter. Like 1-wk GH action, 6-h (i.e. short-term) GH action also increased liver expression of GHR1A and total GHR mRNAs in cattle. These observations together suggest that GH directly stimulates the expression of one GHR mRNA variant, GHR1A, through binding STAT5 to its promoter, thereby increasing GHR mRNA and protein expression in the bovine liver.en
dc.description.sponsorshipNational Institutes of Health (NIH) Grants DK67961, DK46395en
dc.description.sponsorshipVeterans Affairs Merit Reviewen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationHonglin Jiang, Ying Wang, Miaozong Wu, Zhiliang Gu, Stuart J. Frank, and Roberto Torres-Diaz. "Growth Hormone Stimulates Hepatic Expression of Bovine Growth Hormone Receptor Messenger Ribonucleic Acid through Signal Transducer and Activator of Transcription 5 Activation of a Major Growth Hormone Receptor Gene Promoter," Endocrinology 2007 148:7, 3307-3315. DOI: http://dx.doi.org/10.1210/en.2006-1738en
dc.identifier.doihttps://doi.org/10.1210/en.2006-1738en
dc.identifier.issn0013-7227en
dc.identifier.urihttp://hdl.handle.net/10919/49390en
dc.identifier.urlhttp://press.endocrine.org/doi/abs/10.1210/en.2006-1738en
dc.language.isoenen
dc.publisherEndocrine Societyen
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectovine placental-lactogenen
dc.subjectgh receptoren
dc.subjectfactor-ien
dc.subjecttransgenic miceen
dc.subjectrat-liveren
dc.subjectsomatogenic receptorsen
dc.subjectmicroarray analysisen
dc.subjectadipose-tissueen
dc.subjectbinding-sitesen
dc.subjectstat5ben
dc.subjectendocrinology & metabolismen
dc.titleGrowth hormone stimulates hepatic expression of bovine growth hormone receptor messenger ribonucleic acid through signal transducer and activator of transcription 5 activation of a major growth hormone receptor gene promoteren
dc.title.serialEndocrinologyen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten

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