Astrocytes and Müller Cell Alterations During Retinal Degeneration in a Transgenic Rat Model of Retinitis Pigmentosa

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Title: Astrocytes and Müller Cell Alterations During Retinal Degeneration in a Transgenic Rat Model of Retinitis Pigmentosa
Authors: Fernández Sánchez, Laura | Lax, Pedro | Campello Blasco, Laura | Pinilla Lozano, Isabel | Cuenca, Nicolás
Research Group/s: Neurobiología del Sistema Visual y Terapia de Enfermedades Neurodegenerativas (NEUROVIS) | Genética Humana y de Mamíferos (GHM)
Center, Department or Service: Universidad de Alicante. Departamento de Fisiología, Genética y Microbiología | Universidad de Alicante. Instituto Multidisciplinar para el Estudio del Medio "Ramón Margalef"
Keywords: Astrocytes | Müller cells | Gliosis | Immunolabeling | P23H | Retinal remodeling
Knowledge Area: Biología Celular | Fisiología
Issue Date: 22-Dec-2015
Publisher: Frontiers
Citation: Fernández-Sánchez L, Lax P, Campello L, Pinilla I and Cuenca N (2015) Astrocytes and Müller Cell Alterations During Retinal Degeneration in a Transgenic Rat Model of Retinitis Pigmentosa. Front. Cell. Neurosci. 9:484. doi: 10.3389/fncel.2015.00484
Abstract: Purpose: Retinitis pigmentosa includes a group of progressive retinal degenerative diseases that affect the structure and function of photoreceptors. Secondarily to the loss of photoreceptors, there is a reduction in retinal vascularization, which seems to influence the cellular degenerative process. Retinal macroglial cells, astrocytes, and Müller cells provide support for retinal neurons and are fundamental for maintaining normal retinal function. The aim of this study was to investigate the evolution of macroglial changes during retinal degeneration in P23H rats. Methods: Homozygous P23H line-3 rats aged from P18 to 18 months were used to study the evolution of the disease, and SD rats were used as controls. Immunolabeling with antibodies against GFAP, vimentin, and transducin were used to visualize macroglial cells and cone photoreceptors. Results: In P23H rats, increased GFAP labeling in Müller cells was observed as an early indicator of retinal gliosis. At 4 and 12 months of age, the apical processes of Müller cells in P23H rats clustered in firework-like structures, which were associated with ring-like shaped areas of cone degeneration in the outer nuclear layer. These structures were not observed at 16 months of age. The number of astrocytes was higher in P23H rats than in the SD matched controls at 4 and 12 months of age, supporting the idea of astrocyte proliferation. As the disease progressed, astrocytes exhibited a deteriorated morphology and marked hypertrophy. The increase in the complexity of the astrocytic processes correlated with greater connexin 43 expression and higher density of connexin 43 immunoreactive puncta within the ganglion cell layer (GCL) of P23H vs. SD rat retinas. Conclusions: In the P23H rat model of retinitis pigmentosa, the loss of photoreceptors triggers major changes in the number and morphology of glial cells affecting the inner retina.
Sponsor: This research was supported by grants from the Spanish Ministry of Economy and Competitiveness-FEDER (BFU2012-36845), Instituto de Salud Carlos III (RETICS-FEDER RD12/0034/0010), Organización Nacional de Ciegos Españoles (ONCE), and FUNDALUCE.
URI: http://hdl.handle.net/10045/52290
ISSN: 1662-5102
DOI: 10.3389/fncel.2015.00484
Language: eng
Type: info:eu-repo/semantics/article
Rights: © 2015 Fernández-Sánchez, Lax, Campello, Pinilla and Cuenca. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Peer Review: si
Publisher version: http://dx.doi.org/10.3389/fncel.2015.00484
Appears in Collections:INV - NEUROVIS - Artículos de Revistas
INV - GHM - Artículos de Revistas

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