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Article: Apical proteins stimulate complement synthesis by cultured human proximal tubular epithelial cells

TitleApical proteins stimulate complement synthesis by cultured human proximal tubular epithelial cells
Authors
Issue Date1999
PublisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.org
Citation
Journal Of The American Society Of Nephrology, 1999, v. 10 n. 1, p. 69-76 How to Cite?
AbstractThere is increasing evidence to suggest that the renal tubular epithelium is important in the pathogenesis of progressive renal failure resulting from persistent proteinuria. The role of complement in the progression of chronic renal failure is not well defined. The purpose of this study was to characterize the production of complement by human proximal tubular epithelial cells exposed to serum proteins at the apical surface. Complement C3 gene expression was analyzed by reverse transcription and PCR. C3 protein biosynthesis was confirmed by metabolic labeling followed by immunoprecipitation and quantified by enzyme-linked immunosorbent assay. In the quiescent state, proximal tubular epithelial cells grown on permeable membrane supports secreted C3 predominantly into the apical medium. The addition of 5 mg/ml serum proteins led to an 8.9-fold increase in basolateral C3 secretion and a 2.1-fold increase in apical C3 secretion, altering the ratio of basolateral: apical C3 secretion from 0.44 ± 0.16 to 1.87 ± 0.52. C3 mRNA expression was also upregulated in a time- and dose-dependent manner. Serum fractionation demonstrated that the stimulant responsible for these effects was in the molecular weight range 30 to 100 kD. The observed phenomenon was not reproduced when purified human albumin alone was used as the stimulant. These findings could provide a possible mechanism for the link between proteinuria and interstitial fibrosis. This may have potential implications for strategies directed against complement in retarding the progression of chronic renal failure.
Persistent Identifierhttp://hdl.handle.net/10722/162317
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, Sen_US
dc.contributor.authorSheerin, NSen_US
dc.contributor.authorZhou, Wen_US
dc.contributor.authorBrown, Zen_US
dc.contributor.authorSacks, SHen_US
dc.date.accessioned2012-09-05T05:18:56Z-
dc.date.available2012-09-05T05:18:56Z-
dc.date.issued1999en_US
dc.identifier.citationJournal Of The American Society Of Nephrology, 1999, v. 10 n. 1, p. 69-76en_US
dc.identifier.issn1046-6673en_US
dc.identifier.urihttp://hdl.handle.net/10722/162317-
dc.description.abstractThere is increasing evidence to suggest that the renal tubular epithelium is important in the pathogenesis of progressive renal failure resulting from persistent proteinuria. The role of complement in the progression of chronic renal failure is not well defined. The purpose of this study was to characterize the production of complement by human proximal tubular epithelial cells exposed to serum proteins at the apical surface. Complement C3 gene expression was analyzed by reverse transcription and PCR. C3 protein biosynthesis was confirmed by metabolic labeling followed by immunoprecipitation and quantified by enzyme-linked immunosorbent assay. In the quiescent state, proximal tubular epithelial cells grown on permeable membrane supports secreted C3 predominantly into the apical medium. The addition of 5 mg/ml serum proteins led to an 8.9-fold increase in basolateral C3 secretion and a 2.1-fold increase in apical C3 secretion, altering the ratio of basolateral: apical C3 secretion from 0.44 ± 0.16 to 1.87 ± 0.52. C3 mRNA expression was also upregulated in a time- and dose-dependent manner. Serum fractionation demonstrated that the stimulant responsible for these effects was in the molecular weight range 30 to 100 kD. The observed phenomenon was not reproduced when purified human albumin alone was used as the stimulant. These findings could provide a possible mechanism for the link between proteinuria and interstitial fibrosis. This may have potential implications for strategies directed against complement in retarding the progression of chronic renal failure.en_US
dc.languageengen_US
dc.publisherAmerican Society of Nephrology. The Journal's web site is located at http://www.jasn.orgen_US
dc.relation.ispartofJournal of the American Society of Nephrologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshComplement C3 - Biosynthesis - Geneticsen_US
dc.subject.meshEpithelial Cells - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshKidney Failure, Chronic - Etiologyen_US
dc.subject.meshKidney Tubules, Proximal - Drug Effects - Metabolismen_US
dc.subject.meshPermeabilityen_US
dc.subject.meshProteinuria - Complicationsen_US
dc.subject.meshRna, Messenger - Biosynthesisen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshSerum Albumin - Pharmacologyen_US
dc.titleApical proteins stimulate complement synthesis by cultured human proximal tubular epithelial cellsen_US
dc.typeArticleen_US
dc.identifier.emailTang, S:scwtang@hku.hken_US
dc.identifier.authorityTang, S=rp00480en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid9890311en_US
dc.identifier.scopuseid_2-s2.0-0032951121en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032951121&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume10en_US
dc.identifier.issue1en_US
dc.identifier.spage69en_US
dc.identifier.epage76en_US
dc.identifier.isiWOS:000077878300009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTang, S=7403437082en_US
dc.identifier.scopusauthoridSheerin, NS=6603806215en_US
dc.identifier.scopusauthoridZhou, W=7404515807en_US
dc.identifier.scopusauthoridBrown, Z=7005805131en_US
dc.identifier.scopusauthoridSacks, SH=7103294121en_US

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