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Article: Serum from minimal change patients in relapse increases CD80 expression in cultured podocytes

TitleSerum from minimal change patients in relapse increases CD80 expression in cultured podocytes
Authors
Issue Date2013
Citation
Pediatric Nephrology, 2013, v. 28 n. 9, p. 1803-1812 How to Cite?
AbstractBackground: Minimal change disease (MCD) is the most common cause of nephrotic syndrome in children and is associated with the expression of CD80 in podocytes and the increased excretion of CD80 in urine. We hypothesized that serum from patients with MCD might stimulate CD80 expression in cultured podocytes. Methods: Sera and peripheral blood mononuclear cells (PBMCs) were collected from subjects with MCD in relapse and remission and from normal controls. Immortalized human podocytes were incubated with culture media containing patient sera or supernatants from patient and control PBMC cultures. CD80 expression was measured by quantitative PCR and western blot analysis. Results: Sera collected from patients with MCD in relapse, but not in remission, significantly increased CD80 expression (mean ± standard deviation: 1.8 ± 0.7 vs. 0.8 ± 0.2; p < 0.004) and CD80 protein secretion by podocytes (p < 0.05 between relapse and normal controls). No such CD80 increase was observed when podocytes were incubated with supernatants of PBMC cultures from patients in relapse. Conclusions: Sera from MCD patients in relapse, but not in remission, stimulated CD80 expression in cultured podocytes. Identifying this factor in sera could provide insights into the pathogenesis of this disorder. No role in CD80 expression by podocytes was found for cytokines released by PBMCs. © 2013 IPNA.
Persistent Identifierhttp://hdl.handle.net/10722/195522
ISSN
2015 Impact Factor: 2.338
2015 SCImago Journal Rankings: 0.959
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorIshimoto, T-
dc.contributor.authorCara-Fuentes, G-
dc.contributor.authorWang, H-
dc.contributor.authorShimada, M-
dc.contributor.authorWasserfall, CH-
dc.contributor.authorWinter, WE-
dc.contributor.authorRivard, CJ-
dc.contributor.authorAraya, CE-
dc.contributor.authorSaleem, MA-
dc.contributor.authorMathieson, PW-
dc.contributor.authorJohnson, RJ-
dc.contributor.authorGarin, EH-
dc.date.accessioned2014-02-28T06:12:16Z-
dc.date.available2014-02-28T06:12:16Z-
dc.date.issued2013-
dc.identifier.citationPediatric Nephrology, 2013, v. 28 n. 9, p. 1803-1812-
dc.identifier.issn0931-041X-
dc.identifier.urihttp://hdl.handle.net/10722/195522-
dc.description.abstractBackground: Minimal change disease (MCD) is the most common cause of nephrotic syndrome in children and is associated with the expression of CD80 in podocytes and the increased excretion of CD80 in urine. We hypothesized that serum from patients with MCD might stimulate CD80 expression in cultured podocytes. Methods: Sera and peripheral blood mononuclear cells (PBMCs) were collected from subjects with MCD in relapse and remission and from normal controls. Immortalized human podocytes were incubated with culture media containing patient sera or supernatants from patient and control PBMC cultures. CD80 expression was measured by quantitative PCR and western blot analysis. Results: Sera collected from patients with MCD in relapse, but not in remission, significantly increased CD80 expression (mean ± standard deviation: 1.8 ± 0.7 vs. 0.8 ± 0.2; p < 0.004) and CD80 protein secretion by podocytes (p < 0.05 between relapse and normal controls). No such CD80 increase was observed when podocytes were incubated with supernatants of PBMC cultures from patients in relapse. Conclusions: Sera from MCD patients in relapse, but not in remission, stimulated CD80 expression in cultured podocytes. Identifying this factor in sera could provide insights into the pathogenesis of this disorder. No role in CD80 expression by podocytes was found for cytokines released by PBMCs. © 2013 IPNA.-
dc.languageeng-
dc.relation.ispartofPediatric Nephrology-
dc.titleSerum from minimal change patients in relapse increases CD80 expression in cultured podocytes-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s00467-013-2498-4-
dc.identifier.scopuseid_2-s2.0-84881074341-
dc.identifier.volume28-
dc.identifier.issue9-
dc.identifier.spage1803-
dc.identifier.epage1812-
dc.identifier.isiWOS:000322323700012-

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