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Article: Activation of podocytes by mesangial-derived TNF-α: Glomerulo-podocytic communication in IgA nephropathy

TitleActivation of podocytes by mesangial-derived TNF-α: Glomerulo-podocytic communication in IgA nephropathy
Authors
KeywordsMesangial Cell
Tubulointerstitial Injury
Tumor Necrosis Factor-Α
Issue Date2008
Citation
American Journal Of Physiology - Renal Physiology, 2008, v. 294 n. 4, p. F945-F955 How to Cite?
AbstractWe have previously documented that human mesangial cell (HMC)-derived TNF-α is an important mediator involved in the glomerulo-tubular communication in the development of interstitial damage in IgA nephropathy (IgAN). With the strategic position of podocytes, we further examined the role of mesangial cells in the activation of podocytes in IgAN. There was no binding of IgA from patients with IgAN to podocytes. Podocytes cultured with IgA from patients with IgAN did not induce the release of growth factors or cytokines. Furthermore, podocytes did not express mRNA of known IgA receptors. In contrast, IgA-conditioned medium (IgA-HMC medium) prepared by culturing HMC with IgA from patients with IgAN for 48 h significantly increased the gene expression and protein synthesis of TNF-α by podocytes with a 17-fold concentration above that of IgA-HMC medium. The upregulation of TNF-α expression by podocyte was only abolished by a neutralizing antibody against TNF-α but not by other antibodies. Exogenous TNF-α upregulated the synthesis of TNF-α by podocytes in an autocrine fashion. IgA-HMC medium prepared with IgA from patients with IgAN also significantly upregulated the expression of both TNF-α receptor 1 and 2 in podocytes. Our in vitro finding suggests podocytes may play a contributory role in the development of interstitial damage in IgAN by amplifying the activation of tubular epithelial cells with enhanced TNF-α synthesis after inflammatory changes of HMC. Copyright © 2008 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/163175
ISSN
2008 Impact Factor: 3.89
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_US
dc.contributor.authorLeung, JCKen_US
dc.contributor.authorChan, LYYen_US
dc.contributor.authorSaleem, MAen_US
dc.contributor.authorMathieson, PWen_US
dc.contributor.authorLai, FMen_US
dc.contributor.authorTang, SCWen_US
dc.date.accessioned2012-09-05T05:28:26Z-
dc.date.available2012-09-05T05:28:26Z-
dc.date.issued2008en_US
dc.identifier.citationAmerican Journal Of Physiology - Renal Physiology, 2008, v. 294 n. 4, p. F945-F955en_US
dc.identifier.issn0363-6127en_US
dc.identifier.urihttp://hdl.handle.net/10722/163175-
dc.description.abstractWe have previously documented that human mesangial cell (HMC)-derived TNF-α is an important mediator involved in the glomerulo-tubular communication in the development of interstitial damage in IgA nephropathy (IgAN). With the strategic position of podocytes, we further examined the role of mesangial cells in the activation of podocytes in IgAN. There was no binding of IgA from patients with IgAN to podocytes. Podocytes cultured with IgA from patients with IgAN did not induce the release of growth factors or cytokines. Furthermore, podocytes did not express mRNA of known IgA receptors. In contrast, IgA-conditioned medium (IgA-HMC medium) prepared by culturing HMC with IgA from patients with IgAN for 48 h significantly increased the gene expression and protein synthesis of TNF-α by podocytes with a 17-fold concentration above that of IgA-HMC medium. The upregulation of TNF-α expression by podocyte was only abolished by a neutralizing antibody against TNF-α but not by other antibodies. Exogenous TNF-α upregulated the synthesis of TNF-α by podocytes in an autocrine fashion. IgA-HMC medium prepared with IgA from patients with IgAN also significantly upregulated the expression of both TNF-α receptor 1 and 2 in podocytes. Our in vitro finding suggests podocytes may play a contributory role in the development of interstitial damage in IgAN by amplifying the activation of tubular epithelial cells with enhanced TNF-α synthesis after inflammatory changes of HMC. Copyright © 2008 the American Physiological Society.en_US
dc.languageengen_US
dc.relation.ispartofAmerican Journal of Physiology - Renal Physiologyen_US
dc.subjectMesangial Cellen_US
dc.subjectTubulointerstitial Injuryen_US
dc.subjectTumor Necrosis Factor-Αen_US
dc.titleActivation of podocytes by mesangial-derived TNF-α: Glomerulo-podocytic communication in IgA nephropathyen_US
dc.typeArticleen_US
dc.identifier.emailLai, KN:knlai@hku.hken_US
dc.identifier.emailLeung, JCK:jckleung@hku.hken_US
dc.identifier.emailTang, SCW:scwtang@hku.hken_US
dc.identifier.authorityLai, KN=rp00324en_US
dc.identifier.authorityLeung, JCK=rp00448en_US
dc.identifier.authorityTang, SCW=rp00480en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1152/ajprenal.00423.2007en_US
dc.identifier.scopuseid_2-s2.0-44949252210en_US
dc.identifier.hkuros143111-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-44949252210&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume294en_US
dc.identifier.issue4en_US
dc.identifier.spageF945en_US
dc.identifier.epageF955en_US
dc.identifier.isiWOS:000254623200031-
dc.identifier.f1000721990771-
dc.identifier.scopusauthoridLai, KN=7402135706en_US
dc.identifier.scopusauthoridLeung, JCK=7202180349en_US
dc.identifier.scopusauthoridChan, LYY=8108378300en_US
dc.identifier.scopusauthoridSaleem, MA=7103095853en_US
dc.identifier.scopusauthoridMathieson, PW=7005677484en_US
dc.identifier.scopusauthoridLai, FM=7202559720en_US
dc.identifier.scopusauthoridTang, SCW=7403437082en_US

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