ArticleMolecular medicine reports2018
Effects of bradykinin on TGF‑β1‑induced epithelial‑mesenchymal transition in ARPE‑19 cells.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Bone morphogenetic protein-6 suppresses TGF-βInternational journal of ophthalmology · 2024Article
- CD82 attenuates TGF-β1-mediated epithelial-mesenchymal transition by blocking smad-dependent signaling in ARPE-19 cells.Frontiers in pharmacology · 2022Article
- Effects of bradykinin on proliferation, apoptosis, and cycle of glomerular mesangial cells via the TGF-β1/Smad signaling pathway.Turkish journal of biology = Turk biyoloji dergisi · 2021Article
- LRG1 promotes epithelial-mesenchymal transition of retinal pigment epithelium cells by activating NOX4.International journal of ophthalmology · 2021Article
- Involvement of the Retinal Pigment Epithelium in the Development of Retinal Lattice Degeneration.International journal of molecular sciences · 2020Article
- Rosmarinic Acid Attenuates Cadmium-Induced Nephrotoxicity via Inhibition of Oxidative Stress, Apoptosis, Inflammation and Fibrosis.International journal of molecular sciences · 2019Article
- miR‑127 aggravates myocardial failure by promoting the TGF‑β1/Smad3 signaling.Molecular medicine reports · 2018Article
- Quercetin inhibits transforming growth factor β1-induced epithelial-mesenchymal transition in human retinal pigment epithelial cells via the Smad pathway.Drug design, development and therapy · 2018Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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‑β1 (TGF‑β1). 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‑β1 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 α‑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‑β1 resulted in the expression of factors associated with EMT in ARPE‑19 cells. BK decreased the expression levels of the mesenchymal markers α‑SMA and vimentin, and increased the expression of the epithelial marker E‑cadherin. BK decreased cell migration in TGF‑β1‑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‑β1‑treated ARPE‑19 cells, and the protective alterations produced by BK were inhibited by HOE‑140. In conclusion, 10 ng/ml TGF‑β1 resulted in EMT in ARPE‑19 cells and BK served a negative role in TGF‑β1‑induced EMT. BK had effects in TGF‑β1‑induced EMT by upregulating the expression of Smad7 and downregulating the expression of pSmad3 in TGF‑β/Smad signaling pathway, indicating that BK may be a novel and effective therapy for PVR.
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