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Inflammatory mediators of proliferative vitreoretinopathy: hypothesis and review.

ABSTRACT: 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-?, platelet-derived growth factor, interleukin-6, interleukin-8 and tumor necrosis factor-? 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.

SUBMITTER: Dai Y

PROVIDER: S-EPMC7242233 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Inflammatory mediators of proliferative vitreoretinopathy: hypothesis and review.

Dai Ying Y Dai Chenghua C Sun Tao T

International ophthalmology 20200226 6

<h4>Purpose</h4>To review the role of inflammatory mediators in proliferative vitreoretinopathy (PVR) development and the current treatment for PVR prevention.<h4>Methods</h4>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.<h4>Results</h4>Inflammatory mediators, namely growth factors and cytokines, have been ...[more]

PMID: 32103371

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Project description:Purpose: The development of vitreoretinal scars remains an unsolved challenge in clinical practice and often leads to repeated revision surgery and blindness due to lack of efficient therapy. The aim of this study was to characterize the cellular and molecular environment in vitreoretinal scar tissue from patients with proliferative vitreoretinopathy (PVR) in comparison to membranes of the vitreoretinal junction, in order to subsequently identify potential drug treatment options using bioinformatics techniques. Methods: A total of 23 patients undergoing vitrectomy for retinal detachment due to proliferative vitreoretinopathy (PVR, n = 15), idiopathic macular hole (MH, n = 10) or idiopathic macular pucker (MP, n = 8), were included in this study. Vitreoretinal samples were analysed by RNA sequencing, MS-CyTOF proteomic and by conventional immunohistochemistry. The cellular microenvironment was assessed by bioinformatics cell type enrichment analysis. Drug target screening was performed by using a transcriptome-based drug-repurposing approach using drug-exposure transcriptome data from public available databases. Results: RNA sequencing of vitreoretinal tissue samples showed distinct transcriptional differences of PVR, ERM and ILM samples allowing an accurate clustering according to the tissue types. The cellular microenvironment of PVR membranes was characterized by the enrichment of melanocytes, astrocytes and various immune cell types, such as M2 macrophages. Differential gene expression (DEG) analysis revealed XX up- and XX downregulated genes in PVR compared to ILM. Among them, FN1 (fibronectin1), SPARC (osteonectin) and various collagens were among the most upregulated factors in PVR, contributing to biological processes such as the organization of extracellular structures, the regulation of cell adhesion and the morphogenesis of blood vessels. Finally, we identified 13 drugs that induce a gene expression profile complementary to the PVR signature and thus represent potential therapeutic options for PVR, including aminocaproic acid and various topoisomerase 2A inhibitors such as doxorubicin, etoposide and mitoxantrone. Conclusion: The present study reveals significant differences in the transcriptional signature of vitreoretinal scar tissue including PVR, MP and ILM tissue. Among a plethora of differentially expressed genes, FN1 and SPARC appeared to be central mediators underlying PVR development. Based on the transcriptome analyses, aminocaproic acid and topoisomerase-2 inhibitors, such as doxorubicin, etoposide and mitoxantrone, were identified as compatible drugs for the treatment of PVR.

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Inflammatory mediators of proliferative vitreoretinopathy: hypothesis and review.

Publications

Inflammatory mediators of proliferative vitreoretinopathy: hypothesis and review.

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