The aberrant glycosylation of IgA1 is pivotal in the pathogenesis of IgA nephropathy (IgAN). The aim of the present study was to investigate the effect of transforming growth factorβ1 (TGFβ1) on the glycosylation of IgA1 and the associated mechanism. The mRNA levels of core1 β1,
3-galactosyltransferase (C1GalT1) and its molecular chaperone, Cosmc, were analyzed, as was the subsequent O-glycosylation of IgA1, in a human Bcell line stimulated with TGFβ1. The IgA1positive human Bcell line was cultured with different concentrations of recombinant human TGFβ1
(5, 10, 15 and 30 ng/ml). The production and glycosylation of IgA1 were assayed using sandwich ELISA and enzymelinked lectin binding assays, respectively, and the mRNA levels of C1GalT1 and Cosmc were quantified using reverse transcriptionquantitative polymerase chain reaction
analysis. The results showed that the production of IgA1 was stimulated by low concentrations of TGFβ1 (5 or 10 ng/ml) and was suppressed by high concentrations (15 or 30 ng/ml). The terminal glycosylation of secreted IgA1 was altered in response to TGFβ1.
TGFβ1 stimulation significantly decreased the mRNA levels of C1GalT1 and Cosmc. TGFβ1 may be key in controlling the glycosylation of IgA1, in part via the downregulation of C1GalT1 and Cosmc.
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Document Type: Research Article
Department of Nephrology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China
Department of Nephrology, Affiliated Jiujiang Hospital of Nanchang University, Jiujiang, Jiangxi 332000, P.R. China
Institute of Microbiology, Jiangxi Academy of Sciences, Nanchang, Jiangxi 330096, P.R. China
Publication date: January 1, 2017
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Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
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