Abstract
Müller glia are responsible for the neural retina regeneration observed in fish and amphibians throughout life. Despite the presence of these cells in the adult human retina, there is no evidence of regeneration occurring in humans following disease or injury. It may be possible that factors present in the degenerated retina could prevent human Müller glia from proliferating and neurally differentiating within the diseased retina. On this basis, investigations into the proteomic profile of these cells and the abundance of key proteins associated to Müller glia in the gliotic PVR retina, may assist in the identification of factors with the potential to control Müller proliferation and neural differentiation in vivo. Label free mass spectrometry identified 1527 proteins in Müller glial cell preparations, 1631 proteins in normal retina and 1074 in gliotic PVR retina. Compared to normal retina, 28 proteins were upregulated and 196 proteins downregulated by 2-fold or more in the gliotic PVR retina. As determined by comparative proteomic analyses, of the proteins highly upregulated in the gliotic PVR retina, the most highly abundant proteins in Müller cell lysates included vimentin, GFAP, polyubiquitin and HSP90a. The observations that proteins highly upregulated in the gliotic retina constitute major proteins expressed by Müller glia provide the basis for further studies into mechanisms that regulate their production. In addition investigations aimed at controlling the expression of these proteins may aid in the identification of factors that could potentially promote endogenous regeneration of the adult human retina after disease or injury.
Highlights
A common characteristic of retinal degeneration is reactive gliosis, a term coined to describe a process where Müller glia rapidly proliferate (Dyer and Cepko, 2000), undergo morphological changes (Lewis and Fisher, 2003), and release pro-inflammatory and regulatory factors into the local retinal environment (Bringmann et al, 2009)
Proteomic profiles of Müller glial cell lines and of normal and gliotic human retina examined by label free analysis
This study compared the protein expression profile of Müller glia with that of normal and gliotic proliferative vitreo-retinopathy (PVR) human retina and identified changes in cytoskeletal related proteins, extracellular matrix proteins and ribosomal proteins that occur during retinal gliosis
Summary
A common characteristic of retinal degeneration is reactive gliosis, a term coined to describe a process where Müller glia rapidly proliferate (Dyer and Cepko, 2000), undergo morphological changes (Lewis and Fisher, 2003), and release pro-inflammatory and regulatory factors into the local retinal environment (Bringmann et al, 2009). This process, thought to protect the retina from further damage, is not always beneficial and can lead to the formation of glial scarring which further aggravates retinal degeneration (Bringmann and Wiedemann, 2012). For unknown developmental reasons, they are prevented from exerting this
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