Does Arkadia contribute to TGF-β1-induced IgA expression through up-regulation of Smad signaling in IgA nephropathy?

Abstract:

:Immunoglobulin A nephropathy (IgAN) is an immune-complex-mediated glomerulonephritis characterized by the presence of IgA deposits in mesangial and paramesangial regions. However, the exact mechanism involved in IgA deposition is still unknown. TGF-β(1) that mediates the progression of IgAN is well established as a critical IgA class (isotype) switching factor, and Smad proteins are critical intracellular mediators in the expression of TGF-β(1)-targeted genes, which suggest that TGF-β signaling has been implicated in the primary pathogenesis of IgAN. Arkadia, an E3 ubiquitin ligase, can amplify TGF-β signaling through regulating Smads degradation. When these findings are considered together, it is of interest to explore how Arkadia and Smad signaling affect TGF-β(1)-induced IgA expression in IgAN. Therefore, we propose that Arkadia could positively contribute to TGF-β(1)-induced IgA secretion through up-regulation of Smad signaling in the pathogenesis of IgAN.

journal_name

Int Urol Nephrol

authors

Li XZ,Feng JT,Hu CP,Chen ZQ

doi

10.1007/s11255-009-9682-2

subject

Has Abstract

pub_date

2010-09-01 00:00:00

pages

719-22

issue

3

eissn

0301-1623

issn

1573-2584

journal_volume

42

pub_type

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