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Molecular pathogenesis of rhegmatogenous retinal detachment

ABSTRACT: Here, we performed molecular pathology analysis of the vitreous proteomes collected from 127 patients with RRD using SWATH-mass spectrometry. For comparison, samples of neurodegenerative vitreoretinal interface eyes (MH, Pucker) and proliferative diabetic retinopathy eyes with tractional-retinal detachment (PDR-TRD) were used as a control.

INSTRUMENT(S): TripleTOF 6600

ORGANISM(S): Human

SUBMITTER: Tiina ?hman

PROVIDER: MSV000086412 | MassIVE | Thu Nov 05 04:00:00 GMT 2020

REPOSITORIES: MassIVE

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Project description:The vitreous humor can provide important information about physiological and pathophysiological processes within the eye, particularly concerning the retina. Despite the widespread prevalence of various vitreoretinal diseases, that can ultimately lead to blindness, there is not a clear understanding of many molecular processes underlying these conditions. Diabetic retinopathy (DR) is the leading cause of blindness among working-age adults in U.S. and developed world. It can result in macular edema and tractional retinal detachment (TRD). Hyperglycemia can induce damage to retinal cells and capillary closure, leading to retinal ischemia and elevated levels of nitric oxide (NO). This, in turn, increases the activity of protein kinase C and the levels of different growth factors, including vascular endothelial growth factor (VEGF). These events can stimulate the development of new blood vessels from existing matured vessels, which are subsequently encompassed by glial cells and fibrous proliferation, potentially leading to TRD. Rhegmatogenous retinal detachment (RD) is the separation of neuroretinal layers from the retinal pigment epithelium (RPE), induced by a break in the neuroretina that allows the influx of liquefied vitreous. In the detached retina outer layers become ischemic and photoreceptors undergo cell death mainly by apoptosis. Moreover, 3–4 days after retinal detachment, a peak of proliferation of non-neuronal cells, such as astrocytes, endothelial cells, pericytes, and microglia, can be observed. A possible complication of rhegmatogenous retinal detachment is proliferative vitreoretinopathy (PVR), a condition defined by the growth and contraction of cellular membranes within the vitreous cavity. Fibroblast or fibrocyte cells have been detected in epiretinal membranes in PVR, and the origin of these cells is debated. Different authors have suggested that they could be transformed RPE cells or metaplastic vascular endothelial cells, glial cells, macrophages, or hyalocytes. Macular pucker is a condition defined by an epiretinal membrane described as a semi-translucent avascular membrane over the internal limiting membrane (ILM) on the surface of the retina. It can be idiopathic or secondary to various conditions, such as trauma, intraocular inflammation, etc. The initial event that can induce an idiopathic pucker is posterior vitreous detachment (PVD), which can cause dehiscence in the internal limiting membrane. Through this opening, microglial cells move to the preretinal surface, where they can interact with hyalocytes and laminocytes. Subsequent transdifferentiation to fibroblast-like cells leads to the development of an epiretinal membrane.

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Molecular pathogenesis of rhegmatogenous retinal detachment

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