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Article: Mesangial expression of angiotensin II receptor in IgA nephropathy and its regulation by polymeric IgA1

TitleMesangial expression of angiotensin II receptor in IgA nephropathy and its regulation by polymeric IgA1
Authors
KeywordsAngiotensin II
Angiotensin II subtype-1 receptor
Angiotensin II subtype-2 receptor
IgA nephropathy
Mesangial cells
Polymeric IgA
Issue Date2004
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, 2004, v. 66 n. 4, p. 1403-1416 How to Cite?
AbstractBackground. Enhanced gene expression for the renin-angiotensin system (RAS) is detected in glomerular mesangial cells in IgA nephropathy (IgAN). Preliminary studies showed a reduced glomerular gene expression of angiotensin II subtype 1 receptor (AT1R), suggesting a regulatory response to high intrarenal angiotensin II (Ang II) concentration in IgAN. Methods. We examined the effect of polymeric IgA1 (pIgA1) from patients with IgAN on the expression of Ang II receptors in cultured human mesangial cells (HMC). Results. Polymeric IgA1 from patients with IgAN down-regulated the expression of AT1R in HMC in a dose-dependent manner. When similar experiments were conducted with addition of an angiotensin-converting enzyme inhibitor (captopril) or an AT1R antagonist (losartan), there was a significant increase in the expression of AT1R. Blockade of Ang II with captopril or losartan alone resulted in a stepwise increase of AT1R in cultured HMC. Down-regulation of Ang II subtype 2 receptor (AT2R) was not observed in HMC cultured with pIgA1 from patients with IgAN. The acute suppressive effect of pIgA1 from IgAN on the expression of AT1R was confirmed in HMC incubated with IgA isolated from 15 IgAN patients, 15 healthy subjects, and other glomerulonephritides control subjects. Reduced glomerular expression of AT1R (but not AT2R) was also demonstrated in renal biopsies from patients with IgAN. Conclusion. Our findings demonstrate an altered AT1R expression in HMC in response to raised intrarenal Ang II in IgAN. Our in vitro studies also support that ah an imbalance of AT1R and AT2R activity in HMC following exposure to pIgA plays a significant pathogenetic role in the inflammatory injury in IgAN.
Persistent Identifierhttp://hdl.handle.net/10722/78399
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorTang, SCWen_HK
dc.contributor.authorTsang, AWLen_HK
dc.contributor.authorLi, FFKen_HK
dc.contributor.authorLam, MFen_HK
dc.contributor.authorLui, SLen_HK
dc.contributor.authorLeung, JCKen_HK
dc.date.accessioned2010-09-06T07:42:27Z-
dc.date.available2010-09-06T07:42:27Z-
dc.date.issued2004en_HK
dc.identifier.citationKidney International, 2004, v. 66 n. 4, p. 1403-1416en_HK
dc.identifier.issn0085-2538en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78399-
dc.description.abstractBackground. Enhanced gene expression for the renin-angiotensin system (RAS) is detected in glomerular mesangial cells in IgA nephropathy (IgAN). Preliminary studies showed a reduced glomerular gene expression of angiotensin II subtype 1 receptor (AT1R), suggesting a regulatory response to high intrarenal angiotensin II (Ang II) concentration in IgAN. Methods. We examined the effect of polymeric IgA1 (pIgA1) from patients with IgAN on the expression of Ang II receptors in cultured human mesangial cells (HMC). Results. Polymeric IgA1 from patients with IgAN down-regulated the expression of AT1R in HMC in a dose-dependent manner. When similar experiments were conducted with addition of an angiotensin-converting enzyme inhibitor (captopril) or an AT1R antagonist (losartan), there was a significant increase in the expression of AT1R. Blockade of Ang II with captopril or losartan alone resulted in a stepwise increase of AT1R in cultured HMC. Down-regulation of Ang II subtype 2 receptor (AT2R) was not observed in HMC cultured with pIgA1 from patients with IgAN. The acute suppressive effect of pIgA1 from IgAN on the expression of AT1R was confirmed in HMC incubated with IgA isolated from 15 IgAN patients, 15 healthy subjects, and other glomerulonephritides control subjects. Reduced glomerular expression of AT1R (but not AT2R) was also demonstrated in renal biopsies from patients with IgAN. Conclusion. Our findings demonstrate an altered AT1R expression in HMC in response to raised intrarenal Ang II in IgAN. Our in vitro studies also support that ah an imbalance of AT1R and AT2R activity in HMC following exposure to pIgA plays a significant pathogenetic role in the inflammatory injury in IgAN.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.htmlen_HK
dc.relation.ispartofKidney Internationalen_HK
dc.subjectAngiotensin IIen_HK
dc.subjectAngiotensin II subtype-1 receptoren_HK
dc.subjectAngiotensin II subtype-2 receptoren_HK
dc.subjectIgA nephropathyen_HK
dc.subjectMesangial cellsen_HK
dc.subjectPolymeric IgAen_HK
dc.subject.meshApoptosis - physiologyen_HK
dc.subject.meshBiopsyen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshGene Expressionen_HK
dc.subject.meshGlomerular Mesangium - immunology - pathology - physiopathologyen_HK
dc.subject.meshGlomerulonephritis, IGA - immunology - pathology - physiopathologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunoglobulin A - metabolism - pharmacologyen_HK
dc.subject.meshReceptor, Angiotensin, Type 1 - genetics - metabolismen_HK
dc.subject.meshReceptor, Angiotensin, Type 2 - genetics - metabolismen_HK
dc.subject.meshRenin-Angiotensin System - physiologyen_HK
dc.titleMesangial expression of angiotensin II receptor in IgA nephropathy and its regulation by polymeric IgA1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0085-2538&volume=66&spage=1403&epage=1416&date=2004&atitle=Mesangial+expression+of+angiotensin+II+receptor+in+IgA+nephropathy+and+its+regulation+by+polymeric+IgA1en_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailTang, SCW: scwtang@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityTang, SCW=rp00480en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1523-1755.2004.00874.xen_HK
dc.identifier.pmid15458433-
dc.identifier.scopuseid_2-s2.0-4644250240en_HK
dc.identifier.hkuros99276en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-4644250240&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume66en_HK
dc.identifier.issue4en_HK
dc.identifier.spage1403en_HK
dc.identifier.epage1416en_HK
dc.identifier.isiWOS:000223821000011-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridChan, LYY=8108378300en_HK
dc.identifier.scopusauthoridTang, SCW=7403437082en_HK
dc.identifier.scopusauthoridTsang, AWL=7006979244en_HK
dc.identifier.scopusauthoridLi, FFK=55210612400en_HK
dc.identifier.scopusauthoridLam, MF=35300050600en_HK
dc.identifier.scopusauthoridLui, SL=7102379130en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK

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