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Article: Crosstalk between peroxisome proliferator-activated receptor-γ and angiotensin II in renal tubular epithelial cells in IgA nephropathy

TitleCrosstalk between peroxisome proliferator-activated receptor-γ and angiotensin II in renal tubular epithelial cells in IgA nephropathy
Authors
Xiao, JLeung, JCKChan, LYYTang, SCWLai, KN
KeywordsAngiotensin II
Angiotensin II type 1 receptor
Peroxisome proliferator-activated receptor-γ
Tubulointerstitial injury
Issue Date2009
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yclim
Citation
Clinical Immunology, 2009, v. 132 n. 2, p. 266-276 How to Cite?
DOI: http://dx.doi.org/10.1016/j.clim.2009.04.004
AbstractOur recent study suggested that peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist attenuates inflammatory response in activated tubular epithelial cells in IgA nephropathy (IgAN). Here, we explore thiazolidinediones as new therapeutic additives to established treatment regime of renin angiotensin blockade in IgAN. Human proximal tubular epithelial cells (PTEC) were pretreated with PPAR-γ agonist, rosiglitazone, and/or angiotensin II (AngII) type 1 receptor (ATR1) blocker (ARB), losartan, followed by activation with the conditioned medium collected from human mesangial cells incubated with pIgA1 (IgA-HMC) from patients with IgAN. IgA-HMC conditioned medium up-regulated expression of ICAM-1, IL-6 and ATR1 and activated NF-κB and ERK1/2 in PTEC. Dual treatment of rosiglitazone and losartan provided synergistic effect in reducing ICAM-1, IL-6 and ATR1 expression and NF-κB and ERK1/2 activation induced by the conditioned media when compared with monotherapy. Our data suggest that rosiglitazone trans-represses AngII signaling and may offer additional potential when combined with ARB in treating IgAN. © 2009 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/78143
ISSN
1521-6616
2021 Impact Factor: 10.190
2020 SCImago Journal Rankings: 1.236
ISI Accession Number ID
WOS:000268269500013
Funding AgencyGrant Number
Research Grant Council of Hong KongHKU 7661/06M
L & T Charitable Foundation
House of INDOCAFE
Funding Information:

This work was supported by the Research Grant Council (grant number HKU 7661/06M) of Hong Kong. Rosiglitazone was a kind gift from GlaxoSmithKline (Herts, UK). Dr. Loretta Chan was partly supported by L & T Charitable Foundation and the House of INDOCAFE.

References
References in Scopus
Grants
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DC FieldValueLanguage
dc.contributor.authorXiao, Jen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T07:39:38Z-
dc.date.available2010-09-06T07:39:38Z-
dc.date.issued2009en_HK
dc.identifier.citationClinical Immunology, 2009, v. 132 n. 2, p. 266-276en_HK
dc.identifier.issn1521-6616en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78143-
dc.description.abstractOur recent study suggested that peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist attenuates inflammatory response in activated tubular epithelial cells in IgA nephropathy (IgAN). Here, we explore thiazolidinediones as new therapeutic additives to established treatment regime of renin angiotensin blockade in IgAN. Human proximal tubular epithelial cells (PTEC) were pretreated with PPAR-γ agonist, rosiglitazone, and/or angiotensin II (AngII) type 1 receptor (ATR1) blocker (ARB), losartan, followed by activation with the conditioned medium collected from human mesangial cells incubated with pIgA1 (IgA-HMC) from patients with IgAN. IgA-HMC conditioned medium up-regulated expression of ICAM-1, IL-6 and ATR1 and activated NF-κB and ERK1/2 in PTEC. Dual treatment of rosiglitazone and losartan provided synergistic effect in reducing ICAM-1, IL-6 and ATR1 expression and NF-κB and ERK1/2 activation induced by the conditioned media when compared with monotherapy. Our data suggest that rosiglitazone trans-represses AngII signaling and may offer additional potential when combined with ARB in treating IgAN. © 2009 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yclimen_HK
dc.relation.ispartofClinical Immunologyen_HK
dc.subjectAngiotensin IIen_HK
dc.subjectAngiotensin II type 1 receptoren_HK
dc.subjectPeroxisome proliferator-activated receptor-γen_HK
dc.subjectTubulointerstitial injuryen_HK
dc.subject.meshAngiotensin II Type 1 Receptor Blockers - pharmacology-
dc.subject.meshEpithelial Cells - cytology - drug effects - metabolism-
dc.subject.meshGlomerulonephritis, IGA - immunology - metabolism - physiopathology-
dc.subject.meshPPAR gamma - agonists - physiology-
dc.subject.meshReceptor, Angiotensin, Type 1 - genetics - metabolism - physiology-
dc.titleCrosstalk between peroxisome proliferator-activated receptor-γ and angiotensin II in renal tubular epithelial cells in IgA nephropathyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1521-6616&volume=132&issue=2&spage=266&epage=276&date=2009&atitle=Crosstalk+between+peroxisome+proliferator-activated+receptor-γ+and+angiotensin+II+in+renal+tubular+epithelial+cells+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.doi10.1016/j.clim.2009.04.004en_HK
dc.identifier.pmid19443277-
dc.identifier.scopuseid_2-s2.0-67649964290en_HK
dc.identifier.hkuros161037en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67649964290&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume132en_HK
dc.identifier.issue2en_HK
dc.identifier.spage266en_HK
dc.identifier.epage276en_HK
dc.identifier.isiWOS:000268269500013-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectnull-
dc.identifier.scopusauthoridXiao, J=54887023900en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridChan, LYY=55182644100en_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.citeulike5352841-
dc.identifier.issnl1521-6616-

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