Role and Mechanism of Epithelial-Mesenchymal Transition Mediated by Inflammatory Stress-Induced TGF-β1 in Promoting Arteriovenous Fistula Stenosis.

Abstract

To explore the role and mechanism of epithelial-mesenchymal transition (EMT) mediated by inflammatory stress-induced TGF-β1 in promoting arteriovenous fistula stenosis. The inflammatory cells HK-2 were cultured by adding TGF-β1. The optimal stimulation time was determined after TGF-β1 was added. HK-2 cells were divided into two groups, DMEM/F12 medium was added to one group (the control group), and the other group was treated with TGF-β1 (10 ng/ml) in serum-free DMEM/F12 medium to stimulate cell differentiation to mesenchymal. TGF-β1 was stably expressed after being transfected into EMT. The expression of TGF-β1 in the experimental group was higher than that in the control group (P < 0.05) 7 days after transfection. Western blot showed that TGF-β1 protein expression was higher in the experimental group 7 days after transfection, and no TGF-β1 protein expression was detected in the control group. The smooth muscle cells showed α-SMA expression in the control group, but no cells with expression of SMA and CD31/vWF were found at the same time; α-SMA expression was shown in smooth muscle cells and proliferative myofibroblasts, but no cells with expressions of SMA and CD31/vWF were found at the same time. The observation group showed that the expression of α-SMA was detected in smooth muscle cells and proliferative myofibroblasts, CD31/vWF was also expressed in endothelial cells, and α-SMA and vWF were also observed in endothelial cells, but no CD31 expression was found. The inflammatory stress-induced TGF-β1 could act on epithelial-mesenchymal transition and promote the degree of arteriovenous fistula stenosis.