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Article: Increased mRNA encoding for transforming factor-β in CD4+ cells from patients with IgA nephropathy

TitleIncreased mRNA encoding for transforming factor-β in CD4+ cells from patients with IgA nephropathy
Authors
Issue Date1994
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.html
Citation
Kidney International, 1994, v. 46 n. 3, p. 862-868 How to Cite?
AbstractIgA nephropathy (IgAN) is a mesangial proliferative glomerulonephritis characterized by predominant mesangial IgA deposits. Recently, transforming growth factor-β (TGF-β) is shown to exert widespread effects on extracellular matrix by enhancing its accumulation. In an experimental model of acute mesangial glomerulonephritis TGF-β appeared to be involved in the process of glomerulosclerosis, and treatment with antagonists of TGF-β prevented the development of glomerulosclerosis. We examined the TGF-β mRNA expression by mitogen activated CD4+ T cells from 31 patients with IgAN), 25 healthy controls and 10 patients with minimal change nephropathy (MCN) or focal glomerulonephritis (FGN) who were comparable in age and sex. The cytokine gene was analyzed with reverse transcription followed by polymerase chain reaction and was semiquantitated by normalizing the differences occurring during reverse transcription and polymerase chain reaction using a housekeeping gene, p-actin. CD4+ T cells from IgA nephritic patients expressed a higher level of TGF-β mRNA than that of healthy controls or that of MCN/FGN [TGF-β/actin ratio 1.11 (median), range 0.24 to 3.87 vs. 0.88, range 0.2 to 3.83, P = 0.0157 and 0.36 range 0.09 to 1.6, P = 0.006]. When the biopsies were classified into three grades according to the severity of glomerular and interstitial pathology, there were highly significant differences between the TGF-β mRNA in CD4+ T cells from the three groups of IgA nephritic patients (grade 11 0.52, range 0.24 to 0.79; grade 2, 1.2, range 0.5 to 3.33; grade 3, 2.17, range 1.45 to 3.87]. Furthermore, immunofluorescent reactivity of anti-TGF-β antibody in the mesangium was associated with the severity of histopathologic grading (P < 0.05). Our data suggest that, in addition to the local synthesis of TGF-β by mesangial cells, there is increased TGF-β gene expression in circulating CD4+ T cells that may also contribute to the glomerulosclerosis in IgA nephropathy.
Persistent Identifierhttp://hdl.handle.net/10722/162032
ISSN
2015 Impact Factor: 7.683
2015 SCImago Journal Rankings: 3.181
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLai, KNen_HK
dc.contributor.authorHo, RTHen_HK
dc.contributor.authorLeung, JCKen_HK
dc.contributor.authorMacMoune Lai, Fen_HK
dc.contributor.authorLi, PKTen_HK
dc.date.accessioned2012-09-05T05:16:47Z-
dc.date.available2012-09-05T05:16:47Z-
dc.date.issued1994en_HK
dc.identifier.citationKidney International, 1994, v. 46 n. 3, p. 862-868en_HK
dc.identifier.issn0085-2538en_HK
dc.identifier.urihttp://hdl.handle.net/10722/162032-
dc.description.abstractIgA nephropathy (IgAN) is a mesangial proliferative glomerulonephritis characterized by predominant mesangial IgA deposits. Recently, transforming growth factor-β (TGF-β) is shown to exert widespread effects on extracellular matrix by enhancing its accumulation. In an experimental model of acute mesangial glomerulonephritis TGF-β appeared to be involved in the process of glomerulosclerosis, and treatment with antagonists of TGF-β prevented the development of glomerulosclerosis. We examined the TGF-β mRNA expression by mitogen activated CD4+ T cells from 31 patients with IgAN), 25 healthy controls and 10 patients with minimal change nephropathy (MCN) or focal glomerulonephritis (FGN) who were comparable in age and sex. The cytokine gene was analyzed with reverse transcription followed by polymerase chain reaction and was semiquantitated by normalizing the differences occurring during reverse transcription and polymerase chain reaction using a housekeeping gene, p-actin. CD4+ T cells from IgA nephritic patients expressed a higher level of TGF-β mRNA than that of healthy controls or that of MCN/FGN [TGF-β/actin ratio 1.11 (median), range 0.24 to 3.87 vs. 0.88, range 0.2 to 3.83, P = 0.0157 and 0.36 range 0.09 to 1.6, P = 0.006]. When the biopsies were classified into three grades according to the severity of glomerular and interstitial pathology, there were highly significant differences between the TGF-β mRNA in CD4+ T cells from the three groups of IgA nephritic patients (grade 11 0.52, range 0.24 to 0.79; grade 2, 1.2, range 0.5 to 3.33; grade 3, 2.17, range 1.45 to 3.87]. Furthermore, immunofluorescent reactivity of anti-TGF-β antibody in the mesangium was associated with the severity of histopathologic grading (P < 0.05). Our data suggest that, in addition to the local synthesis of TGF-β by mesangial cells, there is increased TGF-β gene expression in circulating CD4+ T cells that may also contribute to the glomerulosclerosis in IgA nephropathy.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ki/index.htmlen_HK
dc.relation.ispartofKidney Internationalen_HK
dc.subject.meshAdulten_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshCd4-Positive T-Lymphocytes - Metabolismen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDna Primersen_US
dc.subject.meshFemaleen_US
dc.subject.meshFluorescent Antibody Techniqueen_US
dc.subject.meshGene Expressionen_US
dc.subject.meshGlomerulonephritis, Iga - Metabolism - Pathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoglobulin A - Analysisen_US
dc.subject.meshLymphocyte Activationen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshRna, Messenger - Metabolismen_US
dc.subject.meshTransforming Growth Factor Beta - Genetics - Metabolismen_US
dc.titleIncreased mRNA encoding for transforming factor-β in CD4+ cells from patients with IgA nephropathyen_HK
dc.typeArticleen_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailHo, RTH: tinho@hku.hken_HK
dc.identifier.emailLeung, JCK: jckleung@hku.hken_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityHo, RTH=rp00497en_HK
dc.identifier.authorityLeung, JCK=rp00448en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/ki.1994.343-
dc.identifier.pmid7996808-
dc.identifier.scopuseid_2-s2.0-0028068363en_HK
dc.identifier.volume46en_HK
dc.identifier.issue3en_HK
dc.identifier.spage862en_HK
dc.identifier.epage868en_HK
dc.identifier.isiWOS:A1994PC21700033-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridHo, RTH=8620896500en_HK
dc.identifier.scopusauthoridLeung, JCK=7202180349en_HK
dc.identifier.scopusauthoridMacMoune Lai, F=6701570301en_HK
dc.identifier.scopusauthoridLi, PKT=25928016800en_HK

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