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Article: Osmotic response element-binding protein (OREBP) is an essential regulator of the urine concentrating mechanism

TitleOsmotic response element-binding protein (OREBP) is an essential regulator of the urine concentrating mechanism
Authors
Issue Date2004
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2004, v. 279 n. 46, p. 48048-48054 How to Cite?
AbstractOREBP (osmotic response element-binding protein), also called TonEBP or NFAT5, is thought to induce the expression of genes that increase the accumulation of organic osmolytes to protect cells against a hypertonic environment. To investigate the consequences of lacking OREBP activity, transgenic (Tg) mice that overexpress OREBPdn (dominant negative form of OREBP) specifically in the epithelial cells of the renal collecting tubules were generated. These mice showed impairment in their urine concentrating mechanism, most likely due to reduced expression of the aquaporin AQP2 and the urea transporter UT-A1 and UT-A2 mRNAs. When deprived of water or after the administration of a vasopressin analogue, urine osmolality of the Tg mice was significantly increased but not to the same extent as that of the wild type mice. The expression of AQP2 and UT-A1, but not UT-A2 mRNAs, was increased to the same level as that of the wild type mice in the water deprivation state, indicating that the vasopressin regulatory mechanism was not affected by OREBPdn. These data indicate that in addition to vasopressin, OREBP is another essential regulator of the urine concentrating mechanism. Furthermore, the OREBPdn Tg mice developed progressive hydronephrosis soon after weaning, confirming the osmoprotective function of OREBP implicated by the in vitro experiments.
Persistent Identifierhttp://hdl.handle.net/10722/146636
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLam, AKMen_HK
dc.contributor.authorKo, BCBen_HK
dc.contributor.authorTam, Sen_HK
dc.contributor.authorMorris, Ren_HK
dc.contributor.authorYang, JYen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorChung, SSMen_HK
dc.date.accessioned2012-05-08T03:21:26Z-
dc.date.available2012-05-08T03:21:26Z-
dc.date.issued2004en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2004, v. 279 n. 46, p. 48048-48054en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146636-
dc.description.abstractOREBP (osmotic response element-binding protein), also called TonEBP or NFAT5, is thought to induce the expression of genes that increase the accumulation of organic osmolytes to protect cells against a hypertonic environment. To investigate the consequences of lacking OREBP activity, transgenic (Tg) mice that overexpress OREBPdn (dominant negative form of OREBP) specifically in the epithelial cells of the renal collecting tubules were generated. These mice showed impairment in their urine concentrating mechanism, most likely due to reduced expression of the aquaporin AQP2 and the urea transporter UT-A1 and UT-A2 mRNAs. When deprived of water or after the administration of a vasopressin analogue, urine osmolality of the Tg mice was significantly increased but not to the same extent as that of the wild type mice. The expression of AQP2 and UT-A1, but not UT-A2 mRNAs, was increased to the same level as that of the wild type mice in the water deprivation state, indicating that the vasopressin regulatory mechanism was not affected by OREBPdn. These data indicate that in addition to vasopressin, OREBP is another essential regulator of the urine concentrating mechanism. Furthermore, the OREBPdn Tg mice developed progressive hydronephrosis soon after weaning, confirming the osmoprotective function of OREBP implicated by the in vitro experiments.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.subject.meshAnimalsen_US
dc.subject.meshAquaporin 2en_US
dc.subject.meshAquaporins - Genetics - Metabolismen_US
dc.subject.meshDna-Binding Proteins - Genetics - Metabolismen_US
dc.subject.meshEpithelial Cells - Cytology - Metabolismen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshKidney - Cytology - Metabolism - Pathologyen_US
dc.subject.meshKidney Concentrating Ability - Physiologyen_US
dc.subject.meshKidney Tubules, Collecting - Cytology - Metabolismen_US
dc.subject.meshMembrane Transport Proteins - Genetics - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshMice, Inbred Cbaen_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshNfatc Transcription Factorsen_US
dc.subject.meshOsmotic Pressureen_US
dc.subject.meshPhenotypeen_US
dc.subject.meshSignal Transduction - Physiologyen_US
dc.subject.meshTranscription Factors - Genetics - Metabolismen_US
dc.subject.meshUrine - Chemistryen_US
dc.subject.meshVasopressins - Chemistry - Metabolismen_US
dc.subject.meshWater - Administration & Dosage - Metabolismen_US
dc.titleOsmotic response element-binding protein (OREBP) is an essential regulator of the urine concentrating mechanismen_HK
dc.typeArticleen_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1074/jbc.M407224200en_HK
dc.identifier.pmid15347663-
dc.identifier.scopuseid_2-s2.0-9144269048en_HK
dc.identifier.hkuros106047-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-9144269048&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume279en_HK
dc.identifier.issue46en_HK
dc.identifier.spage48048en_HK
dc.identifier.epage48054en_HK
dc.identifier.isiWOS:000224957000076-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLam, AKM=7201848036en_HK
dc.identifier.scopusauthoridKo, BCB=7102833927en_HK
dc.identifier.scopusauthoridTam, S=7202037323en_HK
dc.identifier.scopusauthoridMorris, R=7404059338en_HK
dc.identifier.scopusauthoridYang, JY=8915077600en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK

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