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Article: Modulation of calmodulin gene expression as a novel mechanism for growth hormone feedback control by insulin-like growth factor in grass carp pituitary cells

TitleModulation of calmodulin gene expression as a novel mechanism for growth hormone feedback control by insulin-like growth factor in grass carp pituitary cells
Authors
KeywordsCalcineurin
Calmidazolium
Calmodulin
Gene Expression
Grass Carp
Growth Hormone
Insulin-like Growth Factor
Pituitary Cells
Issue Date2005
PublisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.org
Citation
Endocrinology, 2005, v. 146 n. 9, p. 3821-3835 How to Cite?
AbstractCalmodulin (CaM), the Ca2+ sensor in living cells, is essential for biological functions mediated by Ca2+-dependent mechanisms. However, modulation of CaM gene expression at the pituitary level as a means to regulate pituitary hormone synthesis has not been characterized. Here we examined the functional role of CaM in the feedback control of growth hormone (GH) by insulin-like growth factor (IGF) using grass carp pituitary cells as a cell model. To establish the structural identity of CaM expressed in the grass carp, a CaM cDNA, CaM-L, was isolated from the carp pituitary using 3′/5′ RACE. The ORF of this cDNA encodes a 149 a.a. protein sharing the same primary structure with CaMs reported in mammals, birds, and amphibians. This CaM cDNA is phylogenetically related to the CaM I gene family and its transcripts are ubiquitously expressed in the grass carp. In carp pituitary cells, IGF-I and -II induced CaM mRNA expression with a concurrent drop in GH transcript levels. These stimulatory effects on CaM mRNA levels were not mimicked by insulin and appeared to be a direct consequence of IGF activation of CaM gene transcription without altering CaM transcript stability. CaM antagonism and inactivation of calcineurin blocked the inhibitory effects of IGF-I and -II on GH gene expression and CaM over-expression also suppressed the 5′ promoter activity of grass carp GH gene. These results, as a whole, provide evidence for the first time that IGF feedback on GH gene expression is mediated by activation of CaM gene expression at the pituitary level. Copyright © 2005 by The Endocrine Society.
Persistent Identifierhttp://hdl.handle.net/10722/84813
ISSN
2015 Impact Factor: 4.159
2015 SCImago Journal Rankings: 2.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHuo, Len_HK
dc.contributor.authorFu, Gen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorKo, WKWen_HK
dc.contributor.authorWong, AOLen_HK
dc.date.accessioned2010-09-06T08:57:25Z-
dc.date.available2010-09-06T08:57:25Z-
dc.date.issued2005en_HK
dc.identifier.citationEndocrinology, 2005, v. 146 n. 9, p. 3821-3835en_HK
dc.identifier.issn0013-7227en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84813-
dc.description.abstractCalmodulin (CaM), the Ca2+ sensor in living cells, is essential for biological functions mediated by Ca2+-dependent mechanisms. However, modulation of CaM gene expression at the pituitary level as a means to regulate pituitary hormone synthesis has not been characterized. Here we examined the functional role of CaM in the feedback control of growth hormone (GH) by insulin-like growth factor (IGF) using grass carp pituitary cells as a cell model. To establish the structural identity of CaM expressed in the grass carp, a CaM cDNA, CaM-L, was isolated from the carp pituitary using 3′/5′ RACE. The ORF of this cDNA encodes a 149 a.a. protein sharing the same primary structure with CaMs reported in mammals, birds, and amphibians. This CaM cDNA is phylogenetically related to the CaM I gene family and its transcripts are ubiquitously expressed in the grass carp. In carp pituitary cells, IGF-I and -II induced CaM mRNA expression with a concurrent drop in GH transcript levels. These stimulatory effects on CaM mRNA levels were not mimicked by insulin and appeared to be a direct consequence of IGF activation of CaM gene transcription without altering CaM transcript stability. CaM antagonism and inactivation of calcineurin blocked the inhibitory effects of IGF-I and -II on GH gene expression and CaM over-expression also suppressed the 5′ promoter activity of grass carp GH gene. These results, as a whole, provide evidence for the first time that IGF feedback on GH gene expression is mediated by activation of CaM gene expression at the pituitary level. Copyright © 2005 by The Endocrine Society.en_HK
dc.languageengen_HK
dc.publisherThe Endocrine Society. The Journal's web site is located at http://endo.endojournals.orgen_HK
dc.relation.ispartofEndocrinologyen_HK
dc.rightsEndocrinology. Copyright © The Endocrine Society.en_HK
dc.subjectCalcineurinen_HK
dc.subjectCalmidazoliumen_HK
dc.subjectCalmodulinen_HK
dc.subjectGene Expressionen_HK
dc.subjectGrass Carpen_HK
dc.subjectGrowth Hormoneen_HK
dc.subjectInsulin-like Growth Factoren_HK
dc.subjectPituitary Cellsen_HK
dc.titleModulation of calmodulin gene expression as a novel mechanism for growth hormone feedback control by insulin-like growth factor in grass carp pituitary cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0013-7227&volume=146&spage=3821&epage=3835&date=2005&atitle=Modulation+of+Calmodulin+Gene+Expression+as+a+Novel+Mechanism+for+Growth+Hormone+Feedback+Control+by+Insulin-like+Growth+Factor+in+Grass+Carp+Pituitary+Cellsen_HK
dc.identifier.emailWong, AOL: olwong@hkucc.hku.hken_HK
dc.identifier.authorityWong, AOL=rp00806en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1210/en.2004-1508en_HK
dc.identifier.pmid15932934en_HK
dc.identifier.scopuseid_2-s2.0-23844438359en_HK
dc.identifier.hkuros101435en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23844438359&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume146en_HK
dc.identifier.issue9en_HK
dc.identifier.spage3821en_HK
dc.identifier.epage3835en_HK
dc.identifier.isiWOS:000231243600020-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHuo, L=9275343500en_HK
dc.identifier.scopusauthoridFu, G=8670614700en_HK
dc.identifier.scopusauthoridWang, X=8941883500en_HK
dc.identifier.scopusauthoridKo, WKW=7202286890en_HK
dc.identifier.scopusauthoridWong, AOL=7403147570en_HK

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