Smad Anchor for Receptor Activation Regulates High Glucose-Induced EMT via Modulation of Smad2 and Smad3 Activities in Renal Tubular Epithelial Cells.

is an essential adaptor protein in TGF-β1 signaling and it is also involved in the process of Epithelial-mesenchymal transition (EMT) and fibrosis. Our aim was to investigate the effect of on high glucose (HG)-induced EMT and extracellular matrix (ECM) synthesis in renal tubular epithelial cells. METHODS:The cells were transfected with the following plasmids: wild-type duanyu1800 with Smad binding domain deletion) and then subjected to HG ambience (30 mM). The expression levels were assessed by Western-blot, real-time PCR and immunofluorescence. RESULTS:HG-induced EMT phenotype with increased expression of ECM protein in HK-2 cells. This was associated with the decreased expression of duanyu1800 and Smad2. In comparison with the HG group, overexpression of duanyu1800 in HK-2 cells, a relatively high upregulation of ZO-1 expression was seen, while that of Vimentin, fibronectin and collagen I was decreased. The Smad2 protein expression was increased in HK-2 cells after transfection with duanyu1800 (WT) plasmid. Interestingly, the overexpression of duanyu1800 prolonged the activity period of Smad2 and shortened that of Smad3, which seemed consistent with the change of EMT phenotype and ECM changes in HK-2 cell induced by regulates HG-induced EMT and ECM excretion via modulation of the activation of Smad2 and Smad3 in renal tubular epithelial cells. In view of these findings, it is conceivable that duanyu1800 may serve as a potential novel target in pre-EMT states for the amelioration renal fibrosis seen in chronic kidney diseases.

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