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Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Mol+Med+Rep 2018 ; 17 (4): 5878-86 Nephropedia Template TP
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Effects of bradykinin on TGF-?1-induced epithelial-mesenchymal transition in ARPE-19 cells #MMPMID29436636
Wei Q; Liu Q; Ren C; Liu J; Cai W; Zhu M; Jin H; He M; Yu J
Mol Med Rep 2018[Apr]; 17 (4): 5878-86 PMID29436636show ga
The aim of the present study was to investigate the effects of bradykinin (BK) on an epithelial-mesenchymal transition (EMT) model in retinal pigment epithelium (RPE) cells through exposure to transforming growth factor-?1 (TGF-?1). The aim was to improve the effect of BK on proliferative vitreoretinopathy (PVR) progression, and to find a novel method of clinical prevention and treatment for PVR. The morphology of ARPE-19 cells was observed using an inverted phase-contrast microscope. A Cell Counting Kit-8 was used to assess the effects of TGF-?1 on the proliferation of ARPE-19 cells. Western blotting and immunofluorescence were used to detect the expression levels of the epithelial marker E-cadherin, mesenchymal markers ?-smooth muscle actin (SMA) and vimentin, and phosphorylated (p) mothers against decapentaplegic homolog (Smad)3 and Smad7 of the TGF/Smad signaling pathway. Wound healing tests and Transwell assays were performed to detect cell migration ability. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis was performed to detect the expression levels of pSmad3 and Smad7 in the TGF/Smad signaling pathway. The results revealed that the addition of 10 ng/ml TGF-?1 resulted in the expression of factors associated with EMT in ARPE-19 cells. BK decreased the expression levels of the mesenchymal markers ?-SMA and vimentin, and increased the expression of the epithelial marker E-cadherin. BK decreased cell migration in TGF-?1-induced EMT. These effects were reversed by HOE-140, a specific BK 2 receptor antagonist. BK significantly downregulated the expression of pSmad3 and upregulated the expression of Smad7 in TGF-?1-treated ARPE-19 cells, and the protective alterations produced by BK were inhibited by HOE-140. In conclusion, 10 ng/ml TGF-?1 resulted in EMT in ARPE-19 cells and BK served a negative role in TGF-?1-induced EMT. BK had effects in TGF-?1-induced EMT by upregulating the expression of Smad7 and downregulating the expression of pSmad3 in TGF-?/Smad signaling pathway, indicating that BK may be a novel and effective therapy for PVR.