File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: Annexin II on human mesangial cells mediates anti-dsDNA antibody binding

TitleAnnexin II on human mesangial cells mediates anti-dsDNA antibody binding
Authors
KeywordsMedical sciences
Rheumatology
Issue Date2010
PublisherSage Publications Ltd. The Journal's web site is located at http://lup.sagepub.com
Citation
The 9th International Congress on Systemic Lupus Erythematosus (SLE), Vancouver, Canada, 24-27 June 2010. In Lupus, 2010, v. 19 n. 1, suppl., p. 115, abstract no. PO1.M.2 How to Cite?
AbstractOBJECTIVES: Cardinal features of lupus nephritis include the production of anti-dsDNA antibodies, mesangial proliferation and renal inflammation. The mechanism through which anti-dsDNA antibodies might interact with resident renal cells remains to be elucidated. We and others have previously demonstrated that anti-dsDNA antibodies could bind to human mesangial cells (HMC) independent of bridging chromatin material. We further characterized the cross-reactive antigen(s) on HMC which bind human polyclonal anti-ds-DNA antibodies. METHODS: HMC were isolated from renal cortical tissue using differential sieving followed by collagenase treatment. Human polyclonal anti-dsDNA antibodies were isolated from patients with lupus nephritis using Protein A-Sepharose followed by DNA-cellulose affinity chromatography. HMC surface proteins were removed by limited trypsin (10μg/ml) treatment and the binding of anti-dsDNA antibodies to cells assessed by flow cytometry and cellular ELISA. HMC plasma membrane fractions were subjected to Western blot analysis, then probed with purified anti-dsDNA antibodies and subjected to MALDI-TOF spectrometry to identify ‘cross-reactive’ membrane proteins. Renal biopsies were assessed by immunohistochemistry. RESULTS: Limited trypsin but not DNAse treatment of HMC significantly reduced antidsDNA antibody binding (p<0.05). Anti-dsDNA antibodies predominantly bound to a cell surface antigen with a molecular weight of 36kDa and this band was identified as annexin II by MALDI-TOF spectrometry. The binding activity between anti-dsDNA antibodies and annexin II correlated with disease activity. Glomerular annexin II expression was significantly increased in active lupus nephritis (p<0.05), compared with controls and non-lupus kidney diseases. CONCLUSIONS: Our data demonstrated that annexin II on the plasma membrane of HMC mediates anti-dsDNA antibody binding.
DescriptionPoster Presentations - PO1M Pathogenesis: PO1.M.2
Persistent Identifierhttp://hdl.handle.net/10722/126452
ISSN
2015 Impact Factor: 2.118
2015 SCImago Journal Rankings: 0.878

 

DC FieldValueLanguage
dc.contributor.authorCheung, KFen_HK
dc.contributor.authorYung, Sen_HK
dc.contributor.authorChan, DTMen_HK
dc.date.accessioned2010-10-31T12:29:23Z-
dc.date.available2010-10-31T12:29:23Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 9th International Congress on Systemic Lupus Erythematosus (SLE), Vancouver, Canada, 24-27 June 2010. In Lupus, 2010, v. 19 n. 1, suppl., p. 115, abstract no. PO1.M.2en_HK
dc.identifier.issn0961-2033-
dc.identifier.urihttp://hdl.handle.net/10722/126452-
dc.descriptionPoster Presentations - PO1M Pathogenesis: PO1.M.2-
dc.description.abstractOBJECTIVES: Cardinal features of lupus nephritis include the production of anti-dsDNA antibodies, mesangial proliferation and renal inflammation. The mechanism through which anti-dsDNA antibodies might interact with resident renal cells remains to be elucidated. We and others have previously demonstrated that anti-dsDNA antibodies could bind to human mesangial cells (HMC) independent of bridging chromatin material. We further characterized the cross-reactive antigen(s) on HMC which bind human polyclonal anti-ds-DNA antibodies. METHODS: HMC were isolated from renal cortical tissue using differential sieving followed by collagenase treatment. Human polyclonal anti-dsDNA antibodies were isolated from patients with lupus nephritis using Protein A-Sepharose followed by DNA-cellulose affinity chromatography. HMC surface proteins were removed by limited trypsin (10μg/ml) treatment and the binding of anti-dsDNA antibodies to cells assessed by flow cytometry and cellular ELISA. HMC plasma membrane fractions were subjected to Western blot analysis, then probed with purified anti-dsDNA antibodies and subjected to MALDI-TOF spectrometry to identify ‘cross-reactive’ membrane proteins. Renal biopsies were assessed by immunohistochemistry. RESULTS: Limited trypsin but not DNAse treatment of HMC significantly reduced antidsDNA antibody binding (p<0.05). Anti-dsDNA antibodies predominantly bound to a cell surface antigen with a molecular weight of 36kDa and this band was identified as annexin II by MALDI-TOF spectrometry. The binding activity between anti-dsDNA antibodies and annexin II correlated with disease activity. Glomerular annexin II expression was significantly increased in active lupus nephritis (p<0.05), compared with controls and non-lupus kidney diseases. CONCLUSIONS: Our data demonstrated that annexin II on the plasma membrane of HMC mediates anti-dsDNA antibody binding.-
dc.languageengen_HK
dc.publisherSage Publications Ltd. The Journal's web site is located at http://lup.sagepub.com-
dc.relation.ispartofLupus-
dc.rightsLupus. Copyright © Sage Publications Ltd.-
dc.subjectMedical sciences-
dc.subjectRheumatology-
dc.titleAnnexin II on human mesangial cells mediates anti-dsDNA antibody bindingen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0961-2033&volume=19&issue=1, suppl.&spage=115&epage=&date=2010&atitle=Annexin+II+on+human+mesangial+cells+mediates+anti-dsDNA+antibody+binding-
dc.identifier.emailYung, S: ssyyung@hku.hken_HK
dc.identifier.emailChan, DTM: dtmchan@hku.hken_HK
dc.identifier.authorityYung, S=rp00455en_HK
dc.identifier.authorityChan, DTM=rp00394en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1177/09612033100190010101-
dc.identifier.pmid20511279-
dc.identifier.scopuseid_2-s2.0-77953045627-
dc.identifier.hkuros172766en_HK
dc.identifier.volume19-
dc.identifier.issue1, suppl.-
dc.identifier.spage115-
dc.identifier.epage115-
dc.description.otherThe 9th International Congress on Systemic Lupus Erythematosus (SLE), Vancouver, Canada, 24-27 June 2010. In Lupus, 2010, v. 19 n. 1, suppl., p. 115, abstract no. PO1.M.2-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats