Nonsteroid anti-inflammatory therapy suppresses the development of proliferative vitreoretinopathy more effectively than a steroid one

Tikhonovich, Marina; Ердяков, А.К.; Гаврилова, С.А.

doi:10.1007/s10792-017-0594-3

Cited by 12 publications

(11 citation statements)

References 29 publications

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“…ConA is a lectin molecule well studied in the retinal tissue of both invertebrates and vertebrates [53] and used as an adhesive substrate for retinal cells in vitro [86]. Most recently, ConA was used to induce RPC migration from retinal grafts [87] as well as to suppress proliferative vitreoretinopathy in rats [88,89]. Both ConA and PLL have been used as in vitro substrates to examine survival of retinal neurons from amphibians, avians, invertebrates and mammals [86,90].…”

Section: Discussionmentioning

confidence: 99%

Invertebrate Retinal Progenitors as Regenerative Models in a Microfluidic System

Pena

Zhang

Majeska

et al. 2019

Cells

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Regenerative retinal therapies have introduced progenitor cells to replace dysfunctional or injured neurons and regain visual function. While contemporary cell replacement therapies have delivered retinal progenitor cells (RPCs) within customized biomaterials to promote viability and enable transplantation, outcomes have been severely limited by the misdirected and/or insufficient migration of transplanted cells. RPCs must achieve appropriate spatial and functional positioning in host retina, collectively, to restore vision, whereas movement of clustered cells differs substantially from the single cell migration studied in classical chemotaxis models. Defining how RPCs interact with each other, neighboring cell types and surrounding extracellular matrixes are critical to our understanding of retinogenesis and the development of effective, cell-based approaches to retinal replacement. The current article describes a new bio-engineering approach to investigate the migratory responses of innate collections of RPCs upon extracellular substrates by combining microfluidics with the well-established invertebrate model of Drosophila melanogaster. Experiments utilized microfluidics to investigate how the composition, size, and adhesion of RPC clusters on defined extracellular substrates affected migration to exogenous chemotactic signaling. Results demonstrated that retinal cluster size and composition influenced RPC clustering upon extracellular substrates of concanavalin (Con-A), Laminin (LM), and poly-L-lysine (PLL), and that RPC cluster size greatly altered collective migratory responses to signaling from Fibroblast Growth Factor (FGF), a primary chemotactic agent in Drosophila. These results highlight the significance of examining collective cell-biomaterial interactions on bio-substrates of emerging biomaterials to aid directional migration of transplanted cells. Our approach further introduces the benefits of pairing genetically controlled models with experimentally controlled microenvironments to advance cell replacement therapies.

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Section: Discussionmentioning

confidence: 99%

Invertebrate Retinal Progenitors as Regenerative Models in a Microfluidic System

Pena

Zhang

Majeska

et al. 2019

Cells

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“…Thus, these observations have indicated that calcium-independent phospholipase A 2 was associated with the formation of PVR membranes, which might shed light on the treatment of PVR [80]. It is well known that steroid drugs can block the effect of phospholipase A 2 and inhibit the metabolism of arachidonic acid cascade [77].…”

Section: Other Mediators: Arachidonic Acid Metabolitementioning

confidence: 74%

“…Previous studies have confirmed that the expression COX-1 and COX-2 was detectable in the proliferative membranes of PVR patients [79]. At the early stages of PVR development, the administration of lornoxicam, known as nonsteroidal anti-inflammatory drugs (NSAIDs), could not only inhibit the expression of COXs in the retina and choroid, but also reduce the frequency of membrane formation by 31-43% in PVR models [77]. Recent reports have shown that calcium-independent phospholipase A 2 could regulate the proliferation of RPE cells and be identified in most transformed PRE cells in the membranes of PVR patients [80].…”

Section: Other Mediators: Arachidonic Acid Metabolitementioning

confidence: 91%

“…PGD 2 S, known as the key enzyme in the synthesis of prostaglandin D 2 (PGD 2 ), is connected with inflammatory response and retinal apoptosis [76]. It is known that COXs can synthesize prostaglandins from arachidonic acid [77]. On the other hand, prostaglandins can also lead to the increased synthesis of COX-2 by positive feedback mechanism [78].…”

Section: Other Mediators: Arachidonic Acid Metabolitementioning

confidence: 99%

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Inflammatory mediators of proliferative vitreoretinopathy: hypothesis and review

Dai

Sun

2020

Int Ophthalmol

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Purpose To review the role of inflammatory mediators in proliferative vitreoretinopathy (PVR) development and the current treatment for PVR prevention. Methods A PubMed search was carried out using these keywords “PVR,” “inflammatory mediators,” “growth factors,” “cytokines” and “treatment.” Studies regarding inflammatory mediators and PVR therapy were included and published up to December 2019. Results Inflammatory mediators, namely growth factors and cytokines, have been implicated in the occurrence and development of PVR. Among various inflammatory mediators, transforming growth factor-β, platelet-derived growth factor, interleukin-6, interleukin-8 and tumor necrosis factor-α are considered to be particularly important. In this review, we focus on the hypothesis that growth factors and cytokines are involved in the development of PVR, and current treatment for the prevention of PVR. Conclusion We support the hypothesis that growth factors and cytokines may participate in the complex process of PVR development. More importantly, the identification of inflammatory mediators provides novel and efficacious therapeutic targets for the treatment of PVR.

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“…PVR is characterized by proliferation of cells and contraction of membranes within the vitreous cavity and on both sides of the retinal surfaces, which is a common cause of failure in rhegmatogenous retinal detachment surgery (Khan, Brady & Kaiser, 2015). Many attempts have been made in PVR pharmacotherapy (Abdullatif et al, 2018;Tikhonovich, Erdiakov & Gavrilova, 2018), but there are not ideal drugs for PVR treatment because the molecular mechanisms underlying PVR are not well understood. Pathogenesis of PVR is a complex biological process regulated by multiple growth factors and cytokines (Hoerster et al, 2017), and the retinal pigment epithelium (RPE) cells are considered as the key cell type in PVR, which is deemed to proliferate and migrate through retinal breaks (Umazume et al, 2014;Chen et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Icariin affects cell cycle progression and proliferation of human retinal pigment epithelial cells via enhancing expression of H19

Zhang

Han

2020

PeerJ

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Background Aberrant proliferation of retinal pigment epithelial (RPE) cells under pathologic condition results in the occurrence of proliferative vitreoretinopathy (PVR). Icariin (ICA)-a flavonol glucoside-has been shown to inhibit proliferation of many cell types, but the effect on RPE cells is unknown. This study aimed to clarify the inhibitory effects of ICA on RPE cells against platelet-derived growth factor (PDGF)-BB-induced cell proliferation, and discuss the regulatory function of H19 in RPE cells. Methods MTS assay was conducted to determine the effects of ICA on cell proliferation. Flow cytometry analysis was performed to detect cell cycle progression. Quantitative real-time PCR and western blot assay were used to measure the expression patterns of genes in RPE cells. Results ICA significantly suppressed PDGF-BB-stimulated RPE cell proliferation in a concentration-dependent manner. Moreover, since administration of ICA induced cell cycle G0/G1 phase arrest, the anti-proliferative activity of ICA may be due to G0/G1 phase arrest in RPE cells. At molecular levels, cell cycle regulators cyclin D1, CDK4, CDK6, p21 and p53 were modulated in response to treatment with ICA. Most importantly, H19 was positively regulated by ICA and H19 depletion could reverse the inhibitory effects of ICA on cell cycle progression and proliferation in PDGF-BB-stimulated RPE cells. Further mechanical explorations showed that H19 knockdown resulted in alternative expressions levels of cyclin D1, CDK4, CDK6, p21 and p53 under ICA treatment. Conclusions Our findings revealed that ICA was an effective inhibitor of PDGF-BB-induced RPE cell proliferation through affecting the expression levels of cell cycle-associated factors, and highlighted the potential application of ICA in PVR therapy. H19 was described as a target regulatory gene of ICA whose disruption may contribute to excessive proliferation of RPE cells, suggesting that modulation of H19 expression may be a novel therapeutic approach to treat PVR.

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Nonsteroid anti-inflammatory therapy suppresses the development of proliferative vitreoretinopathy more effectively than a steroid one

Cited by 12 publications

References 29 publications

Invertebrate Retinal Progenitors as Regenerative Models in a Microfluidic System

Invertebrate Retinal Progenitors as Regenerative Models in a Microfluidic System

Inflammatory mediators of proliferative vitreoretinopathy: hypothesis and review

Icariin affects cell cycle progression and proliferation of human retinal pigment epithelial cells via enhancing expression of H19

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