Andreas Bringmann1, Peter Wiedemann. 1. Department of Ophthalmology, Faculty of Medicine, University of Leipzig, Eye Hospital, Leipzig, Germany. bria@medizin.uni-leipzig.de
Abstract
BACKGROUND: Proliferative retinopathies are considered to represent maladapted retinal wound repair processes driven by growth factor- and cytokine-induced overstimulation of proliferation, migration, extracellular matrix production and contraction of retinal cells. The formation of neovascular membranes represents an attempt to reoxygenize non-perfused retinal areas. Müller glial cells play a crucial role in the pathogenesis of proliferative retinopathies. This review summarizes the present knowledge regarding the role of Müller cells in periretinal membrane formation, especially in the early steps of epiretinal membrane formation, which involve an interaction of inflammatory and glial cells, and gives a survey of the factors which are suggested to be implicated in the induction of Müller cell gliosis and proliferation. CONCLUSIONS: Alterations in the membrane conductance of Müller cells suggest that Müller cells may alter their phenotype into progenitor-like cells in the course of proliferative retinopathies; transdifferentiated Müller cells may have great impact for the development of new cell-based therapies.
BACKGROUND: Proliferative retinopathies are considered to represent maladapted retinal wound repair processes driven by growth factor- and cytokine-induced overstimulation of proliferation, migration, extracellular matrix production and contraction of retinal cells. The formation of neovascular membranes represents an attempt to reoxygenize non-perfused retinal areas. Müller glial cells play a crucial role in the pathogenesis of proliferative retinopathies. This review summarizes the present knowledge regarding the role of Müller cells in periretinal membrane formation, especially in the early steps of epiretinal membrane formation, which involve an interaction of inflammatory and glial cells, and gives a survey of the factors which are suggested to be implicated in the induction of Müller cell gliosis and proliferation. CONCLUSIONS: Alterations in the membrane conductance of Müller cells suggest that Müller cells may alter their phenotype into progenitor-like cells in the course of proliferative retinopathies; transdifferentiated Müller cells may have great impact for the development of new cell-based therapies.
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