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Article: Increased mesangial cell hyaluronan expression in lupus nephritis is mediated by anti-DNA antibody-induced IL-1β

TitleIncreased mesangial cell hyaluronan expression in lupus nephritis is mediated by anti-DNA antibody-induced IL-1β
Authors
Issue Date2006
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, 2006, v. 69 n. 2, p. 272-280 How to Cite?
AbstractThe mechanism by which anti-DNA antibodies contribute to the pathogenesis of lupus nephritis (LN) remains to be fully elucidated. Hyaluronan (HA) is an important extracellular matrix constituent that accumulates during tissue injury, and participates in lymphocyte recruitment to sites of inflammation. The role of HA in the pathogenesis of LN has not been defined. We investigated the expression of HA in renal biopsies and circulating HA levels in patients with diffuse proliferative LN, and the effect of human anti-DNA antibodies on HA synthesis in cultured human mesangial cells (HMC). HA expression was increased in the mesangium, and in the periglomerular and tubular distribution in LN kidney biopsies. LN patients showed increased levels of circulating HA, especially during active disease, which correlated with anti-DNA antibody titers (r=0.35, P=0.0234). Anti-DNA antibodies isolated during active LN but not remission increased de novo synthesis of 3H-labeled HA, which was accompanied by induction of HA synthase (HAS) II transcription, and enhanced IL-1β, IL-6, and tumor necrosis factor-α secretion in HMC (P<0.001 for all). Only anti-DNA antibody induction of IL-1β enhanced HA synthesis, which was abrogated by inhibitors of de novo mRNA or protein synthesis. Our findings demonstrate that HA expression is significantly increased within the mesangium in diffuse proliferative LN mediated through anti-DNA antibody-induced IL-1β. Given that HA plays a pivotal role during inflammatory responses, influences cellular behavior and assists in the recruitment of lymphocytes to sites of injury, it is likely that HA contributes to the pathogenesis of LN. © 2006 International Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/162944
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYung, Sen_US
dc.contributor.authorTsang, RCWen_US
dc.contributor.authorLeung, JKHen_US
dc.contributor.authorChan, TMen_US
dc.date.accessioned2012-09-05T05:25:39Z-
dc.date.available2012-09-05T05:25:39Z-
dc.date.issued2006en_US
dc.identifier.citationKidney International, 2006, v. 69 n. 2, p. 272-280en_US
dc.identifier.issn0085-2538en_US
dc.identifier.urihttp://hdl.handle.net/10722/162944-
dc.description.abstractThe mechanism by which anti-DNA antibodies contribute to the pathogenesis of lupus nephritis (LN) remains to be fully elucidated. Hyaluronan (HA) is an important extracellular matrix constituent that accumulates during tissue injury, and participates in lymphocyte recruitment to sites of inflammation. The role of HA in the pathogenesis of LN has not been defined. We investigated the expression of HA in renal biopsies and circulating HA levels in patients with diffuse proliferative LN, and the effect of human anti-DNA antibodies on HA synthesis in cultured human mesangial cells (HMC). HA expression was increased in the mesangium, and in the periglomerular and tubular distribution in LN kidney biopsies. LN patients showed increased levels of circulating HA, especially during active disease, which correlated with anti-DNA antibody titers (r=0.35, P=0.0234). Anti-DNA antibodies isolated during active LN but not remission increased de novo synthesis of 3H-labeled HA, which was accompanied by induction of HA synthase (HAS) II transcription, and enhanced IL-1β, IL-6, and tumor necrosis factor-α secretion in HMC (P<0.001 for all). Only anti-DNA antibody induction of IL-1β enhanced HA synthesis, which was abrogated by inhibitors of de novo mRNA or protein synthesis. Our findings demonstrate that HA expression is significantly increased within the mesangium in diffuse proliferative LN mediated through anti-DNA antibody-induced IL-1β. Given that HA plays a pivotal role during inflammatory responses, influences cellular behavior and assists in the recruitment of lymphocytes to sites of injury, it is likely that HA contributes to the pathogenesis of LN. © 2006 International Society of Nephrology.en_US
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.htmlen_US
dc.relation.ispartofKidney Internationalen_US
dc.subject.meshAdulten_US
dc.subject.meshAntibodies, Antinuclear - Physiologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshFemaleen_US
dc.subject.meshGlomerular Mesangium - Cytology - Metabolismen_US
dc.subject.meshGlucuronosyltransferase - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshHyaluronic Acid - Biosynthesisen_US
dc.subject.meshInterleukin-1 - Physiologyen_US
dc.subject.meshLupus Nephritis - Etiology - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.titleIncreased mesangial cell hyaluronan expression in lupus nephritis is mediated by anti-DNA antibody-induced IL-1βen_US
dc.typeArticleen_US
dc.identifier.emailYung, S:ssyyung@hku.hken_US
dc.identifier.emailChan, TM:dtmchan@hku.hken_US
dc.identifier.authorityYung, S=rp00455en_US
dc.identifier.authorityChan, TM=rp00394en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.ki.5000042en_US
dc.identifier.pmid16408116-
dc.identifier.scopuseid_2-s2.0-33644661974en_US
dc.identifier.hkuros117894-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33644661974&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume69en_US
dc.identifier.issue2en_US
dc.identifier.spage272en_US
dc.identifier.epage280en_US
dc.identifier.eissn1523-1755-
dc.identifier.isiWOS:000234843100015-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridYung, S=22636568800en_US
dc.identifier.scopusauthoridTsang, RCW=36808555100en_US
dc.identifier.scopusauthoridLeung, JKH=36857921300en_US
dc.identifier.scopusauthoridChan, TM=7402687700en_US

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