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Inhibition of TGF-β1-receptor posttranslational core fucosylation attenuates rat renal interstitial fibrosis.

著者 Shen N , Lin H , Wu T , Wang D , Wang W , Xie H , Zhang J , Feng Z
Kidney Int.2013 Jul ; 84(1):64-77.
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The profibrotic cytokine transforming growth factor-β1 (TGF-β1) causes renal fibrosis by binding to receptors at the cell surface; however, it is not clear which of the TGF-β superfamily receptors correlates with renal fibrosis. To resolve this, we quantified TGF-β superfamily receptor expression in the kidneys of rats with unilateral ureteral obstruction using a real-time PCR gene array. Expression of activin receptor-like kinase (ALK)-5, ALK7, and TGF-β receptor II (TGF-βRII) mRNA increased significantly, while ALK6 mRNA expression was significantly decreased in the obstructed rat kidney. Core fucosylation is essential for the proper function of both TGF-βRII and ALK5 in cultured human renal proximal tubular epithelial cells in vitro. Therefore, we targeted posttranslational core fucosylation, regulated by α-1,6 fucosyltransferase (FUT8), by adenoviral-mediated knockdown of FUT8 mRNA in vivo and measured TGF-βRII and ALK5 expression and the progression of renal fibrosis. Despite long-term obstruction injury, inhibition of TGF-βRII and ALK5 of core fucosylation ameliorated the progression of renal fibrosis, an effect independent of TGF-βRII and ALK5 expression. Thus, the regulation of TGF-β1-receptor core fucosylation may provide a novel potential therapeutic strategy for treating renal fibrosis.
PMID: 23486519 [PubMed - indexed for MEDLINE]
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