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

Abstract

Objective. To explore the role and mechanism of epithelial-mesenchymal transition (EMT) mediated by inflammatory stress-induced TGF-β1 in promoting arteriovenous fistula stenosis. Methods. 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. Results. 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. Conclusion. The inflammatory stress-induced TGF-β1 could act on epithelial-mesenchymal transition and promote the degree of arteriovenous fistula stenosis

Effect of umbilical cord mesenchymal stem cells on hypoxia-inducible factor-1 alpha (HIF-1α) production in arteriovenous fistula (AVF) animal model: A preliminary study

“…One possible mechanism is that the transplanted stem cells release factors or cytokines that promote angiogenesis and vasculogenesis, thereby enhancing the formation of new blood vessels in the AVF. These newly formed blood vessels may support the delivery of oxygen and nutrients to the surrounding tissues, reducing hypoxia and preventing IH formation [ 20 ]. Another possible mechanism is that UC-MSCs have immunomodulatory properties [ 21 ] which are important factors in IH development by modulating the immune response and can suppress inflammation in the vessel wall [ 22 ].…”

Retracted: Role and Mechanism of Epithelial‐Mesenchymal Transition Mediated by Inflammatory Stress‐Induced TGF‐β1 in Promoting Arteriovenous Fistula Stenosis

“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Peer-review manipulation …”

“…Tis article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. Tis investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”