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Article: Genetic restoration of aldose reductase to the collecting tubules restores maturation of the urine concentrating mechanism

TitleGenetic restoration of aldose reductase to the collecting tubules restores maturation of the urine concentrating mechanism
Authors
KeywordsDiabetes insipidus
Urine concentration
Issue Date2006
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajprenal.physiology.org/
Citation
American Journal Of Physiology - Renal Physiology, 2006, v. 291 n. 1, p. F186-F195 How to Cite?
AbstractTo investigate the underlying causes for aldose reductase deficiency-induced diabetes insipidus, we carried out studies with three genotypic groups of mice. These included wild-type mice, knockout mice, and a newly created bitransgenic line that was homozygous for both the aldose reductase null mutation and an aldose reductase knockin transgene driven by the kidney-specific cadherin promoter to direct transgene expression in the collecting tubule epithelial cells. We found that from early renal developmental stages onward, urine osmolality did not exceed 1,000 mosmol/kgH 2O in aldose reductase-deficient mice. The functional defects were correlated with significant renal cellular and structural abnormalities that included cell shrinkage, apoptosis, disorganized tubular and vascular structures, and segmental atrophy. In contrast, the transgenic aldose reductase expression in the bitransgenic mice largely but incompletely rescued urine concentrating capacity and significantly improved renal cell survival, cellular morphology, and renal structures. Together, these results suggest that aldose reductase not only plays important roles in osmoregulation and medullary cell survival but may also be essential for the full maturation of the urine concentrating mechanism. Copyright © 2006 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/67847
ISSN
2008 Impact Factor: 3.89
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, JYen_HK
dc.contributor.authorTam, WYen_HK
dc.contributor.authorTam, Sen_HK
dc.contributor.authorGuo, Hen_HK
dc.contributor.authorWu, Xen_HK
dc.contributor.authorLi, Gen_HK
dc.contributor.authorChau, JFLen_HK
dc.contributor.authorKlein, JDen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorSands, JMen_HK
dc.contributor.authorChung, SSMen_HK
dc.date.accessioned2010-09-06T05:58:49Z-
dc.date.available2010-09-06T05:58:49Z-
dc.date.issued2006en_HK
dc.identifier.citationAmerican Journal Of Physiology - Renal Physiology, 2006, v. 291 n. 1, p. F186-F195en_HK
dc.identifier.issn0363-6127en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67847-
dc.description.abstractTo investigate the underlying causes for aldose reductase deficiency-induced diabetes insipidus, we carried out studies with three genotypic groups of mice. These included wild-type mice, knockout mice, and a newly created bitransgenic line that was homozygous for both the aldose reductase null mutation and an aldose reductase knockin transgene driven by the kidney-specific cadherin promoter to direct transgene expression in the collecting tubule epithelial cells. We found that from early renal developmental stages onward, urine osmolality did not exceed 1,000 mosmol/kgH 2O in aldose reductase-deficient mice. The functional defects were correlated with significant renal cellular and structural abnormalities that included cell shrinkage, apoptosis, disorganized tubular and vascular structures, and segmental atrophy. In contrast, the transgenic aldose reductase expression in the bitransgenic mice largely but incompletely rescued urine concentrating capacity and significantly improved renal cell survival, cellular morphology, and renal structures. Together, these results suggest that aldose reductase not only plays important roles in osmoregulation and medullary cell survival but may also be essential for the full maturation of the urine concentrating mechanism. Copyright © 2006 the American Physiological Society.en_HK
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajprenal.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Renal Physiologyen_HK
dc.subjectDiabetes insipidusen_HK
dc.subjectUrine concentrationen_HK
dc.subject.meshAldehyde Reductase - analysis - genetics - physiologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAquaporin 2 - analysis - genetics - physiologyen_HK
dc.subject.meshAquaporin 3 - analysis - genetics - physiologyen_HK
dc.subject.meshCell Survival - physiologyen_HK
dc.subject.meshDiabetes Insipidus - genetics - physiopathologyen_HK
dc.subject.meshGene Expression Regulation, Enzymologicen_HK
dc.subject.meshKidney Concentrating Ability - genetics - physiologyen_HK
dc.subject.meshKidney Tubules, Collecting - enzymology - pathology - physiologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMembrane Transport Proteins - analysis - genetics - physiologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshPolyuria - physiopathologyen_HK
dc.subject.meshWater-Electrolyte Balance - physiologyen_HK
dc.titleGenetic restoration of aldose reductase to the collecting tubules restores maturation of the urine concentrating mechanismen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1931-857X&volume=291&spage=F186&epage=F195&date=2006&atitle=Genetic+restoration+of+aldose+reductase+to+the+collecting+tubules+restores+maturation+of+the+urine+concentrating+mechanismen_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_fulltext-
dc.identifier.doi10.1152/ajprenal.00506.2005en_HK
dc.identifier.pmid16449351-
dc.identifier.scopuseid_2-s2.0-33745365627en_HK
dc.identifier.hkuros129010en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745365627&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume291en_HK
dc.identifier.issue1en_HK
dc.identifier.spageF186en_HK
dc.identifier.epageF195en_HK
dc.identifier.isiWOS:000238121900020-
dc.identifier.scopusauthoridYang, JY=8915077600en_HK
dc.identifier.scopusauthoridTam, WY=7102605531en_HK
dc.identifier.scopusauthoridTam, S=7202037323en_HK
dc.identifier.scopusauthoridGuo, H=55468645700en_HK
dc.identifier.scopusauthoridWu, X=7407060267en_HK
dc.identifier.scopusauthoridLi, G=14022821600en_HK
dc.identifier.scopusauthoridChau, JFL=9236841800en_HK
dc.identifier.scopusauthoridKlein, JD=7404605415en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridSands, JM=35597253800en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK

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