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Article: Interaction between the polyol pathway and non-enzymatic glycation on mesangial cell gene expression

TitleInteraction between the polyol pathway and non-enzymatic glycation on mesangial cell gene expression
Authors
KeywordsAdvanced glycation end-products
Aldose reductase gene
Diabetic glomerulopathy
Diabetic nephropathy
TGF-β 1
Transgenic mouse
Type IV collagen
Issue Date2004
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEE
Citation
Nephron - Experimental Nephrology, 2004, v. 98 n. 3, p. e89-e99 How to Cite?
AbstractBackground/Aims: Both activation of the polyol pathway and enhanced non-enzymatic glycation have been implicated in the pathogenesis of diabetic glomerulopathy. We investigated the interaction between these two pathways using normal mesangial cells (MCs) and transgenic (TG) MCs with elevated aldose reductase (AR) activity. Methods: TG mice with expression of the human AR (hAR) gene in kidney MCs were established. Mouse glomeruli and primary cultures of MCs from hAR TG and wild-type (WT) mice were studied regarding the changes in AR activity, transforming growth factor-β 1 (TGF-β 1) and type IV collagen mRNA and protein levels, in response to BSA modified by advanced glycation endproducts (AGE-BSA). Results: Ex vivo addition of AGE-BSA increased AR activity, TGF-β 1 and type IV collagen mRNA levels in both WT and TG glomeruli, with greater rise in TG glomeruli. These increments were attenuated by zopolrestat, an AR inhibitor. In cultured MCs, AGE-BSA enhanced AR activity, TGF-β 1 and type IV collagen mRNA and protein levels both in WT and TG MCs, again with greater increases in TG MCs. The AGE-induced enhancement in TGF-β 1 and type IV collagen expression were suppressed by either zopolrestat or transfection with an AR antisense oligonucleotide. Conclusion: These data suggest that the activation of the polyol pathway by AGEs, more marked in genetic conditions with increased AR activity, may contribute to the pathogenesis of diabetic glomerulopathy, through enhancing mesangial cell expression of TGF-β 1 and type IV collagen. Copyright © 2004 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/76566
ISSN
2015 Impact Factor: 1.531
2015 SCImago Journal Rankings: 1.030
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDan, Qen_HK
dc.contributor.authorWong, RLCen_HK
dc.contributor.authorYin, Sen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorLam, KSLen_HK
dc.date.accessioned2010-09-06T07:22:36Z-
dc.date.available2010-09-06T07:22:36Z-
dc.date.issued2004en_HK
dc.identifier.citationNephron - Experimental Nephrology, 2004, v. 98 n. 3, p. e89-e99en_HK
dc.identifier.issn1660-2129en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76566-
dc.description.abstractBackground/Aims: Both activation of the polyol pathway and enhanced non-enzymatic glycation have been implicated in the pathogenesis of diabetic glomerulopathy. We investigated the interaction between these two pathways using normal mesangial cells (MCs) and transgenic (TG) MCs with elevated aldose reductase (AR) activity. Methods: TG mice with expression of the human AR (hAR) gene in kidney MCs were established. Mouse glomeruli and primary cultures of MCs from hAR TG and wild-type (WT) mice were studied regarding the changes in AR activity, transforming growth factor-β 1 (TGF-β 1) and type IV collagen mRNA and protein levels, in response to BSA modified by advanced glycation endproducts (AGE-BSA). Results: Ex vivo addition of AGE-BSA increased AR activity, TGF-β 1 and type IV collagen mRNA levels in both WT and TG glomeruli, with greater rise in TG glomeruli. These increments were attenuated by zopolrestat, an AR inhibitor. In cultured MCs, AGE-BSA enhanced AR activity, TGF-β 1 and type IV collagen mRNA and protein levels both in WT and TG MCs, again with greater increases in TG MCs. The AGE-induced enhancement in TGF-β 1 and type IV collagen expression were suppressed by either zopolrestat or transfection with an AR antisense oligonucleotide. Conclusion: These data suggest that the activation of the polyol pathway by AGEs, more marked in genetic conditions with increased AR activity, may contribute to the pathogenesis of diabetic glomerulopathy, through enhancing mesangial cell expression of TGF-β 1 and type IV collagen. Copyright © 2004 S. Karger AG, Basel.en_HK
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NEEen_HK
dc.relation.ispartofNephron - Experimental Nephrologyen_HK
dc.rightsNephron Experimental Nephrology. Copyright © S Karger AG.en_HK
dc.subjectAdvanced glycation end-productsen_HK
dc.subjectAldose reductase geneen_HK
dc.subjectDiabetic glomerulopathyen_HK
dc.subjectDiabetic nephropathyen_HK
dc.subjectTGF-β 1en_HK
dc.subjectTransgenic mouseen_HK
dc.subjectType IV collagenen_HK
dc.subject.meshAldehyde Reductase - metabolismen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Culture Techniquesen_HK
dc.subject.meshCollagen Type IV - biosynthesis - physiologyen_HK
dc.subject.meshDiabetic Nephropathies - physiopathologyen_HK
dc.subject.meshGene Expression Regulationen_HK
dc.subject.meshGlycosylation End Products, Advanced - physiologyen_HK
dc.subject.meshKidney Glomerulus - cytology - pathologyen_HK
dc.subject.meshL-Iditol 2-Dehydrogenaseen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshRNA, Messenger - analysis - biosynthesisen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshSerum Albumin, Bovineen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTransforming Growth Factor beta - physiologyen_HK
dc.subject.meshTransforming Growth Factor beta1en_HK
dc.titleInteraction between the polyol pathway and non-enzymatic glycation on mesangial cell gene expressionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1660-2129&volume=98&spage=89&epage=99&date=2004&atitle=Interaction+between+the+polyol+pathway+and+non-enzymatic+glycation+on+mesangial+cell+gene+expressionen_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000080684en_HK
dc.identifier.pmid15528949en_HK
dc.identifier.scopuseid_2-s2.0-8344266747en_HK
dc.identifier.hkuros106060en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-8344266747&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume98en_HK
dc.identifier.issue3en_HK
dc.identifier.spagee89en_HK
dc.identifier.epagee99en_HK
dc.identifier.isiWOS:000224897700004-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridDan, Q=8570225000en_HK
dc.identifier.scopusauthoridWong, RLC=37062742700en_HK
dc.identifier.scopusauthoridYin, S=8979453800en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.citeulike2268756-

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