Retinal detachment with proliferative vitreoretinopathy: surgical results with scleral buckling, closed vitrectomy, and intravitreous air injection.

Ho, Pak‐Chung; McMeel, J. Wallace

doi:10.1136/bjo.69.8.584

Cited by 17 publications

(4 citation statements)

References 14 publications

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“…Vitrectomy techniques have substantially improved surgical results. Most authors have reported anatomically successfully results in 50-80% of cases of RRD with C 1 or more PVR treated by vitrectomy [16][17][18][19].…”

Section: Discussionmentioning

confidence: 99%

Anatomic outcome of scleral buckling surgery in primary rhegmatogenous retinal detachment

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Anatomic outcome of scleral buckling surgery in primary rhegmatogenous retinal detachment

et al. 2006

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“…Proliferative vitreoretinopathy (PVR) is a complication of retinal detachment (RD) and is the primary cause of surgical failure following RD treatment ( 1 ). PVR is characterized by the formation of fibrotic tissue on the detached retina, which hinders retinal reattachment and can potentially cause blindness ( 2 ).…”

Section: Introductionmentioning

confidence: 99%

Novel NADPH oxidase inhibitor VAS2870 suppresses TGF‑β‑dependent epithelial‑to‑mesenchymal transition in retinal pigment epithelial cells

Yang

Wang

et al. 2018

Int J Mol Med

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NADPH oxidases (NOXs) are important in the pathophysiology of fibrotic diseases. The expression and activity of NOXs are regulated by growth factors, including transforming growth factor (TGF-β). The proliferation of retinal pigment epithelial (RPE) cells following epithelial- to-mesenchymal transition (EMT) is a major pathological change involved in proliferative vitreoretinopathy (PVR). The aim of the present study was to determine the effects of the novel NOX inhibitor VAS2870 on the TGF-β-dependent expression of NOX4 and associated cellular events in RPE cells. Cell viability was examined using a Cell Counting Kit-8 assay and cell cycle progression was detected by flow cytometric analysis. Immunofluorescence analysis and western blot analysis were performed to assess EMT. It was found that TGF-β increased the expression of NOX4 and that pre-incubation with VAS2870 eliminated this effect. Additionally, TGF-β promoted RPE migration and increased EMT. Pre-incubation with VAS2870 significantly prevented TGF-β2-induced EMT by decreasing the levels of α-smooth muscle actin and E-cadherin, and also inhibited the migratory ability of the RPE cells, as demonstrated by scratch assays. Finally, VAS2870 suppressed the proliferation of RPE cells, and led to G1-phase cell cycle arrest and a significant downregulation of the expression of cyclin D1. In conclusion, the pharmacological inhibition of NOX may be a promising tool for the treatment of PVR.

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“…Proliferative vitreoretinopathy (PVR) is an active process that develops as a complication during retinal detachment (RD) and it is the most common cause of surgical failure upon RD treatment [ 1 ]. PVR is a dynamic process characterized by the formation of fibrotic tissue on the detached retina, preventing the reattachment of the retina and finally may cause blindness [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

TGF-β1 Induced Transdifferentiation of RPE Cells is Mediated by TAK1

et al. 2015

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Background and AimProliferative vitreoretinopathy (PVR) is an active process that develops as a complication upon retinal detachment (RD), accompanied by formation of fibrotic tissue. The main cells involved in the development of fibrotic tissue during PVR are the retinal pigment epithelial (RPE) cells. The RPE cells undergo epithelial-mesenchymal transition (EMT) which leads to complex retinal detachment and loss of vision. Transforming growth factor-β1 (TGF-β1) is considered as the main player in the EMT of RPE cells, even though the mechanism is not fully understood. This study was performed to determine the possible involvement of transforming growth factor β activated kinase 1 (TAK1) in the EMT process of the RPE cells.MethodologyARPE-19 Cells were treated with 5Z-7 oxozeaenol (TAK1 inhibitor) or SB431542 (TGF-β1 receptor kinase inhibitor) followed by TGF-β1 stimulation. Immunofluorescence, scratch assay Real time PCR and collagen contraction assay assessed the EMT features. The phosphorylation of Smad2/3 and p38 was examined using western blots analysis.ResultsThis study demonstrates that stimulation of RPE cells with TGF-β1 increases α-SMA expression, cell migration and cell contractility, all of which are EMT features. Remarkably, addition of TAK1 inhibitor abolishes all these processes. Furthermore, we show hereby that TAK1 regulates not only the activation of the non-canonical cascade of TGF-β1 (p38), but also the canonical cascade, the Smad2/3 activation. Thus, the outcome of the TGF-β response in RPE cells is TAK1 dependent.Conclusions/SignificanceThis work demonstrated TAK1, a component of the non-canonical pathway of TGF-β1, is a key player in the EMT process, thus provides deep insight into the pathogenesis of PVR. The ability to halt the process of EMT in RPE cells may reduce the severity of the fibrotic response that occurs upon PVR, leading to a better prognosis and increase the probability of success in RD treatment.

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Retinal detachment with proliferative vitreoretinopathy: surgical results with scleral buckling, closed vitrectomy, and intravitreous air injection.

Cited by 17 publications

References 14 publications

Anatomic outcome of scleral buckling surgery in primary rhegmatogenous retinal detachment

Anatomic outcome of scleral buckling surgery in primary rhegmatogenous retinal detachment

Novel NADPH oxidase inhibitor VAS2870 suppresses TGF‑β‑dependent epithelial‑to‑mesenchymal transition in retinal pigment epithelial cells

TGF-β1 Induced Transdifferentiation of RPE Cells is Mediated by TAK1

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