The novel use of decorin in prevention of the development of proliferative vitreoretinopathy (PVR)

Nassar, Khaled; Lüke, Julia; Lüke, Matthias; Kamal, Mohamed; El-Nabi, Effat Abd; Soliman, Mahmoud M.; Rohrbach, Martin; Grisanti, Salvatore

doi:10.1007/s00417-011-1730-9

Cited by 36 publications

(21 citation statements)

References 62 publications

(76 reference statements)

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“…Since EMT and cell migration are associated with the mammalian glial scarring response, elucidating a mechanism by which canonical TGFβ signaling could be inhibited, while allowing for dedifferentiation and non-gliotic proliferation that occurs in adult zebrafish, possibly through corepressors such as Tgif1 and Six3, would be attractive for translational mammalian studies and potential therapeutic treatments for retinal degeneration. Interestingly, decorin, a naturally occurring TGFβ inhibitor, is already used to treat surgical glaucoma patients, and a recent study of rabbit PVR shows that decorin treatment prior to surgery reduces the scarring response (Nassar et al, 2011). …”

Section: Complex Network Of Signaling Pathways Necessary For Regenmentioning

confidence: 99%

Müller glia: Stem cells for generation and regeneration of retinal neurons in teleost fish

Lenkowski

Raymond

2014

Progress in Retinal and Eye Research

276

303

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Adult zebrafish generate new neurons in the brain and retina throughout life. Growth-related neurogenesis allows a vigorous regenerative response to damage, and fish can regenerate retinal neurons, including photoreceptors, and restore functional vision following photic, chemical, or mechanical destruction of the retina. Müller glial cells in fish function as radial-glial-like neural stem cells. During adult growth, Müller glial nuclei undergo sporadic, asymmetric, self-renewing mitotic divisions in the inner nuclear layer to generate a rod progenitor that migrates along the radial fiber of the Müller glia into the outer nuclear layer, proliferates, and differentiates exclusively into rod photoreceptors. When retinal neurons are destroyed, Müller glia in the immediate vicinity of the damage partially and transiently dedifferentiate, re-express retinal progenitor and stem cell markers, re-enter the cell cycle, undergo interkinetic nuclear migration (characteristic of neuroepithelial cells), and divide once in an asymmetric, self-renewing division to generate a retinal progenitor. This daughter cell proliferates rapidly to form a compact neurogenic cluster surrounding the Müller glia; these multipotent retinal progenitors then migrate along the radial fiber to the appropriate lamina to replace missing retinal neurons. Some aspects of the injury-response in fish Müller glia resemble gliosis as observed in mammals, and mammalian Müller glia exhibit some neurogenic properties, indicative of a latent ability to regenerate retinal neurons. Understanding the specific properties of fish Müller glia that facilitate their robust capacity to generate retinal neurons will inform and inspire new clinical approaches for treating blindness and visual loss with regenerative medicine.

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Section: Complex Network Of Signaling Pathways Necessary For Regenmentioning

confidence: 99%

Müller glia: Stem cells for generation and regeneration of retinal neurons in teleost fish

Lenkowski

Raymond

2014

Progress in Retinal and Eye Research

276

303

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“…Antibodies against TGF- β 2 and IL-10, an antagonist of TGF- β , inhibit the contractility of RPE cells on epiretinal membranes [90]. In vivo experiments have shown that decorin, a naturally occurring TGF- β inhibitor, and fasudil, a potent inhibitor of a key downstream mediator of TGF- β called Rho-kinase, may reduce fibrosis and RD development [91–94]. …”

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

117

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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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“…The in vivo evidence on the role of this cytokine in PVR pathogenesis comes from experiments like that by Nassar et al, who used decorin, a naturally occurring TGF-β inhibitor, in a rabbit model of PVR. They found that adjuvant decorin application during vitrectomy reduced fibrosis and RD development 33. Moreover, fasudil, a potent inhibitor of a key downstream mediator of TGF-β called Rho-kinase, was found to significantly inhibit PVR progression in the experimental model without apparent retinal cell toxicity, elucidating the role of TGF-β in this disease 34…”

Section: Pathogenesis and Risk Factorsmentioning

confidence: 99%

Proliferative vitreoretinopathy: current and emerging treatments

Sadaka¹,

Giuliari²

2012

OPTH

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Proliferative vitreoretinopathy is a disease process that follows the proliferation of ectopic cell sheets in the vitreous and/or periretinal area, causing periretinal membrane formation and traction, in patients with rhegmatogenous retinal detachments. Currently, vitreous surgery is the standard treatment; however, the results aren’t satisfactory given the vision loss that ensues and that redetachment is relatively common. It is becoming clearer that there exists an interplay between various cytokines/growth factors, matrix proteins, and the different cell types that drive the undesirable formation of periretinal membranes. This fundamental understanding is aiding in identifying different adjunct agents that can block the cellular events intrinsic to proliferative vitreoretinopathy. In this review, we describe the current understanding on the pathogenesis and discuss how the fundamental understanding of the biochemical/molecular events is instrumental in developing the novel treatment strategies that are also highlighted.

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The novel use of decorin in prevention of the development of proliferative vitreoretinopathy (PVR)

Abstract: In conclusion, in this rabbit model of PVR, adjuvant decorin application during vitrectomy effectively reduces fibrosis and TRD development. In conjunction with no obvious histopathological toxicity signs, decorin represents a promising substance to inhibit PVR reactions.

Cited by 36 publications

References 62 publications

Müller glia: Stem cells for generation and regeneration of retinal neurons in teleost fish

Müller glia: Stem cells for generation and regeneration of retinal neurons in teleost fish

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

Proliferative vitreoretinopathy: current and emerging treatments

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