Wound Healing

Rb, Wilkins; Dr, Kulwin

doi:10.1016/s0161-6420(79)35490-2

Cited by 20 publications

(6 citation statements)

References 2 publications

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“…There is an initial inflammatory phase, a secondary proliferative response, and modulation of the scar which causes contraction [14, 33]. The breakdown of the blood-ocular barrier caused by a retinal break that enables effusion of inflammatory cells (macrophages, leukocytes, and platelets) which release growth factors, including platelet-derived growth factor, TGF-β, and epidermal growth factor [34, 35].…”

Section: Design Of Pvr Animal Models For Pharmaceutical Investigationmentioning

confidence: 99%

Animal Models of Proliferative Vitreoretinopathy and Their Use in Pharmaceutical Investigations

2018

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Section: Design Of Pvr Animal Models For Pharmaceutical Investigationmentioning

confidence: 99%

Animal Models of Proliferative Vitreoretinopathy and Their Use in Pharmaceutical Investigations

2018

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“…These include breakdown of the BRB, chemotaxis and cellular migration, cellular proliferation, membrane formation with remodeling of the extracellular matrix, and contraction [47]. …”

Section: Pathobiology and Pathophysiology Of Pvrmentioning

confidence: 99%

Proliferative Vitreoretinopathy after Eye Injuries: An Overexpression of Growth Factors and Cytokines Leading to a Retinal Keloid

Morescalchi

Duse

Gambicorti

et al. 2013

Mediators of Inflammation

125

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Eye injury is a significant disabling worldwide health problem. Proliferative Vitreoretinopathy (PVR) is a common complication that develops in up to 40–60% of patients with an open-globe injury. Our knowledge about the pathogenesis of PVR has improved in the last decades. It seems that the introduction of immune cells into the vitreous, like in penetrating ocular trauma, triggers the production of growth factors and cytokines that come in contact with intra-retinal cells, like Müller cells and RPE cells. Growth factors and cytokines drive the cellular responses leading to PVR's development. Knowledge of the pathobiological and pathophysiological mechanisms involved in posttraumatic PVR is increasing the possibilities of management, and it is hoped that in the future our treatment strategies will evolve, in particular adopting a multidrug approach, and become even more effective in vision recovery. This paper reviews the current literature and clinical trial data on the pathogenesis of PVR and its correlation with ocular trauma and describes the biochemical/molecular events that will be fundamental for the development of novel treatment strategies. This literature review included PubMed articles published from 1979 through 2013. Only studies written in English were included.

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“…Furthermore, the strong correlation between these cytokine levels and the degree of fibrosis in vitreoretinal disorders suggests that they are important factors in ocular fibrosis and contraction of fibrovascular tissue. Moreover, the interleukins stimulate the proliferation of many types of cell and promote the synthesis of collagen during wound healing [ 49 ]. Park et al demonstrated that the production of EMT-related cytokines, including TGF- β 1, VEGF, IL-6, IL-8, MCP-1, and TNF- α , was approximately 2-fold to 5-fold higher during EMT of ARPE-19 cells [ 41 ].…”

Section: Discussionmentioning

confidence: 99%

Small Interfering RNA Targeted to ASPP2 Promotes Progression of Experimental Proliferative Vitreoretinopathy

Chen

Bai

et al. 2016

Mediators of Inflammation

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Background. Epithelial-mesenchymal transition (EMT) of retinal pigment epithelium (RPE) is vital in proliferative vitreoretinopathy (PVR) development. Apoptosis-stimulating proteins of p53 (ASPP2) have recently been reported to participate in EMT. However, the role of ASPP2 in PVR pathogenesis has not been identified. Methods. Immunohistochemistry was used to investigate the expression of ASPP2 in epiretinal membranes of PVR patients. ARPE-19 cells were transfected with ASPP2-siRNA, followed with measurement of cell cytotoxicity, proliferation, and migration ability. EMT markers and related inflammatory and fibrosis cytokines were measured by western blot or flow cytometry. Additionally, PVR rat models were induced by intravitreal injection of ARPE-19 cells transfected with ASPP2-siRNA and evaluated accordingly. Results. Immunofluorescence analysis revealed less intense expression of ASPP2 in PVR membranes. ASPP2 knockdown facilitated the proliferation and migration of RPE cells and enhanced the expression of mesenchymal markers such as alpha smooth muscle actin, fibronectin, and ZEB1. Meanwhile, ASPP2-siRNA increased EMT-related and inflammatory cytokines, including TGF-β, CTGF, VEGF, TNF-α, and interleukins. PVR severities were more pronounced in the rat models with ASPP2-siRNA treatment. Conclusions. ASPP2 knockdown promoted EMT of ARPE-19 cells in vitro and exacerbated the progression of experimental PVR in vivo, possibly via inflammatory and fibrosis cytokines.

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Wound Healing

Cited by 20 publications

References 2 publications

Animal Models of Proliferative Vitreoretinopathy and Their Use in Pharmaceutical Investigations

Animal Models of Proliferative Vitreoretinopathy and Their Use in Pharmaceutical Investigations

Proliferative Vitreoretinopathy after Eye Injuries: An Overexpression of Growth Factors and Cytokines Leading to a Retinal Keloid

Small Interfering RNA Targeted to ASPP2 Promotes Progression of Experimental Proliferative Vitreoretinopathy

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