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Article: Absence of CD89, polymeric immunoglobulin receptor, and asialoglycoprotein receptor on human mesangial cells

TitleAbsence of CD89, polymeric immunoglobulin receptor, and asialoglycoprotein receptor on human mesangial cells
Authors
Issue Date2000
PublisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.org
Citation
Journal Of The American Society Of Nephrology, 2000, v. 11 n. 2, p. 241-249 How to Cite?
AbstractIgA nephropathy (IgAN) is characterized by raised serum IgA and predominant mesangial IgA deposits of polymeric nature. The expression of IgA receptor molecules in white blood cells and glomerular mesangial cells has recently attracted much attention in relation to the uptake of IgA by these cells. This study investigates the expression of IgA Fc receptor (FcαR1 or CD89), asialoglycoprotein receptor (ASGPR), and polymeric Ig receptor (pIgR) in cultured glomerular mesangial cells. Using a sensitive nested reverse transcription-PCR, mRNA encoding for FcαR1, pIgR, or the H2 chain of ASGPR was not demonstrated on human mesangial cells. U937, HepG2, and HT29 cell lines, used as positive controls, strongly expressed the FcαR1, ASGPR, and pIgR mRNA, respectively, under similar experimental conditions. Flow cytometry also demonstrated the presence of surface proteins for FcαR1, ASGPR, and pIgR on the respective control cell lines but not on human mesangial cells. Expression of FcαR1 mRNA on cultured U937 cells was upregulated by tumor necrosis factor-α. However, tumor necrosis factor-α, interleukin-1β, or transforming growth factor-β failed to induce the expression of FcαR1 on human mesangial cells. Human serum IgA or secretory IgA bound to human mesangial cells, HepG2, or the U937 cell line in a dose- dependent manner. The binding of purified IgA to human mesangial cells was not blocked by preincubation with human IgG, IgM, orosomucoid, asialoorosomucoid, anti-CD89 antibody (My43), or anti-secretory component antibody. The present study concluded that there was an absence of FcαR1, ASGPR, or pIgR on human mesangial cells. These findings suggest that the predominant binding of human IgA to human mesangial cells is mediated by other mechanisms.
Persistent Identifierhttp://hdl.handle.net/10722/162401
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorTsang, AWLen_HK
dc.contributor.authorChan, DTMen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2012-09-05T05:19:36Z-
dc.date.available2012-09-05T05:19:36Z-
dc.date.issued2000en_HK
dc.identifier.citationJournal Of The American Society Of Nephrology, 2000, v. 11 n. 2, p. 241-249en_HK
dc.identifier.issn1046-6673en_HK
dc.identifier.urihttp://hdl.handle.net/10722/162401-
dc.description.abstractIgA nephropathy (IgAN) is characterized by raised serum IgA and predominant mesangial IgA deposits of polymeric nature. The expression of IgA receptor molecules in white blood cells and glomerular mesangial cells has recently attracted much attention in relation to the uptake of IgA by these cells. This study investigates the expression of IgA Fc receptor (FcαR1 or CD89), asialoglycoprotein receptor (ASGPR), and polymeric Ig receptor (pIgR) in cultured glomerular mesangial cells. Using a sensitive nested reverse transcription-PCR, mRNA encoding for FcαR1, pIgR, or the H2 chain of ASGPR was not demonstrated on human mesangial cells. U937, HepG2, and HT29 cell lines, used as positive controls, strongly expressed the FcαR1, ASGPR, and pIgR mRNA, respectively, under similar experimental conditions. Flow cytometry also demonstrated the presence of surface proteins for FcαR1, ASGPR, and pIgR on the respective control cell lines but not on human mesangial cells. Expression of FcαR1 mRNA on cultured U937 cells was upregulated by tumor necrosis factor-α. However, tumor necrosis factor-α, interleukin-1β, or transforming growth factor-β failed to induce the expression of FcαR1 on human mesangial cells. Human serum IgA or secretory IgA bound to human mesangial cells, HepG2, or the U937 cell line in a dose- dependent manner. The binding of purified IgA to human mesangial cells was not blocked by preincubation with human IgG, IgM, orosomucoid, asialoorosomucoid, anti-CD89 antibody (My43), or anti-secretory component antibody. The present study concluded that there was an absence of FcαR1, ASGPR, or pIgR on human mesangial cells. These findings suggest that the predominant binding of human IgA to human mesangial cells is mediated by other mechanisms.en_HK
dc.languageengen_US
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.meshAntibodies - Pharmacologyen_US
dc.subject.meshAntigens, Cd - Genetics - Immunology - Metabolismen_US
dc.subject.meshAsialoglycoprotein Receptoren_US
dc.subject.meshCell Lineen_US
dc.subject.meshCytokines - Pharmacologyen_US
dc.subject.meshGlomerular Mesangium - Cytology - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoglobulin A - Metabolism - Pharmacologyen_US
dc.subject.meshImmunoglobulin A, Secretory - Pharmacologyen_US
dc.subject.meshImmunoglobulin G - Pharmacologyen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshReceptors, Cell Surface - Genetics - Metabolismen_US
dc.subject.meshReceptors, Fc - Genetics - Immunology - Metabolismen_US
dc.subject.meshReceptors, Polymeric Immunoglobulin - Genetics - Metabolismen_US
dc.titleAbsence of CD89, polymeric immunoglobulin receptor, and asialoglycoprotein receptor on human mesangial cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.emailChan, DTM: dtmchan@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.identifier.authorityChan, DTM=rp00394en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.pmid10665931-
dc.identifier.scopuseid_2-s2.0-0033956711en_HK
dc.identifier.hkuros49800-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033956711&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume11en_HK
dc.identifier.issue2en_HK
dc.identifier.spage241en_HK
dc.identifier.epage249en_HK
dc.identifier.isiWOS:000085099500006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridTsang, AWL=7006979244en_HK
dc.identifier.scopusauthoridChan, DTM=7402687700en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

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