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Article: Tubular expression of angiotensin II receptors and their regulation in IgA nephropathy

TitleTubular expression of angiotensin II receptors and their regulation in IgA nephropathy
Authors
Issue Date2005
PublisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.org
Citation
Journal Of The American Society Of Nephrology, 2005, v. 16 n. 8, p. 2306-2317 How to Cite?
AbstractEnhanced renal expression for the renin-angiotensin system (RAS) is detected in IgA nephropathy (IgAN). Previous data showed an altered glomerular expression of angiotensin II type 1 receptor (AT1R), suggesting a regulatory response to high intrarenal angiotensin II (Ang II) concentration in IgAN. In this study, the expression and regulation of Ang II receptors were examined in human proximal tubular epithelial cells (PTEC) in IgAN. Tubular expression of AT1R and Ang II type 2 receptor (AT2R) was increased in IgAN. In vitro culture experiment showed that the upregulation of Ang II receptors was not due to the direct effect of IgA but the indirect effect after IgA deposition on human mesangial cell. When PTEC were cultured with conditioned culture medium from human mesangial cells activated with IgA, Ang II production was upregulated, leading to inflammation and apoptosis via the AT1R and AT2R, respectively. Sequential expression of Ang II receptors determined the injury of PTEC induced by mediators in the conditioned medium. The initial interaction between Ang II and AT1R activated both protein kinase C and mitogen-activated protein kinase pathways, leading to inflammatory responses. This early AT1R-dependent event was followed by upregulation of AT2R expression and continued Ang II release. The interaction between Ang II and AT2R subsequently led to expression of cleaved poly[ADP-ribose] polymerase through downregulation of the mitogen-activated protein kinase pathway. The data suggest that appropriate control of Ang II receptor activities in PTEC may ameliorate tubulointerstitial injury in IgAN. Copyright © 2005 by the American Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/78720
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorChoy, CBYen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T07:45:59Z-
dc.date.available2010-09-06T07:45:59Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of The American Society Of Nephrology, 2005, v. 16 n. 8, p. 2306-2317en_HK
dc.identifier.issn1046-6673en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78720-
dc.description.abstractEnhanced renal expression for the renin-angiotensin system (RAS) is detected in IgA nephropathy (IgAN). Previous data showed an altered glomerular expression of angiotensin II type 1 receptor (AT1R), suggesting a regulatory response to high intrarenal angiotensin II (Ang II) concentration in IgAN. In this study, the expression and regulation of Ang II receptors were examined in human proximal tubular epithelial cells (PTEC) in IgAN. Tubular expression of AT1R and Ang II type 2 receptor (AT2R) was increased in IgAN. In vitro culture experiment showed that the upregulation of Ang II receptors was not due to the direct effect of IgA but the indirect effect after IgA deposition on human mesangial cell. When PTEC were cultured with conditioned culture medium from human mesangial cells activated with IgA, Ang II production was upregulated, leading to inflammation and apoptosis via the AT1R and AT2R, respectively. Sequential expression of Ang II receptors determined the injury of PTEC induced by mediators in the conditioned medium. The initial interaction between Ang II and AT1R activated both protein kinase C and mitogen-activated protein kinase pathways, leading to inflammatory responses. This early AT1R-dependent event was followed by upregulation of AT2R expression and continued Ang II release. The interaction between Ang II and AT2R subsequently led to expression of cleaved poly[ADP-ribose] polymerase through downregulation of the mitogen-activated protein kinase pathway. The data suggest that appropriate control of Ang II receptor activities in PTEC may ameliorate tubulointerstitial injury in IgAN. Copyright © 2005 by the American Society of Nephrology.en_HK
dc.languageengen_HK
dc.publisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.orgen_HK
dc.relation.ispartofJournal of the American Society of Nephrologyen_HK
dc.subject.meshAngiotensin IIen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshCells, Cultured - cytologyen_HK
dc.subject.meshCulture Media, Conditioned - metabolism - pharmacologyen_HK
dc.subject.meshDose-Response Relationship, Drugen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshEnzyme Activationen_HK
dc.subject.meshEpithelial Cells - cytologyen_HK
dc.subject.meshGene Expression Regulationen_HK
dc.subject.meshGlomerulonephritis, IGA - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImidazoles - pharmacologyen_HK
dc.subject.meshImmunoblottingen_HK
dc.subject.meshImmunoglobulin A - chemistry - metabolismen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshInflammationen_HK
dc.subject.meshInterleukin-6 - biosynthesisen_HK
dc.subject.meshKidney Diseases - pathologyen_HK
dc.subject.meshKidney Glomerulus - metabolismen_HK
dc.subject.meshKidney Tubules - cytology - metabolism - pathologyen_HK
dc.subject.meshKineticsen_HK
dc.subject.meshLosartan - pharmacologyen_HK
dc.subject.meshMAP Kinase Signaling Systemen_HK
dc.subject.meshMesangial Cells - cytologyen_HK
dc.subject.meshMitogen-Activated Protein Kinase 1 - metabolismen_HK
dc.subject.meshMitogen-Activated Protein Kinase 3 - metabolismen_HK
dc.subject.meshModels, Biologicalen_HK
dc.subject.meshPoly(ADP-ribose) Polymerases - biosynthesisen_HK
dc.subject.meshProtein Kinase C - metabolismen_HK
dc.subject.meshPyridines - pharmacologyen_HK
dc.subject.meshReceptor, Angiotensin, Type 1 - metabolismen_HK
dc.subject.meshReceptor, Angiotensin, Type 2 - biosynthesis - metabolismen_HK
dc.subject.meshRecombinant Proteins - chemistryen_HK
dc.subject.meshRenin-Angiotensin Systemen_HK
dc.subject.meshSignal Transductionen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshTumor Necrosis Factor-alpha - metabolismen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleTubular expression of angiotensin II receptors and their regulation in IgA nephropathyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1046-6673&volume=16&issue=8&spage=2306&epage=2317&date=2005&atitle=Tubular+expression+of+angiotensin+II+receptors+and+their+regulation+in+IgA+nephropathyen_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1681/ASN.2004121117en_HK
dc.identifier.pmid15930094-
dc.identifier.scopuseid_2-s2.0-28444474540en_HK
dc.identifier.hkuros121279en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-28444474540&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume16en_HK
dc.identifier.issue8en_HK
dc.identifier.spage2306en_HK
dc.identifier.epage2317en_HK
dc.identifier.isiWOS:000230774700009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChan, LYY=8108378300en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridChoy, CBY=9735613000en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

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