ArticlePloS one2015
Müller glia activation in response to inherited retinal degeneration is highly varied and disease-specific.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed, 142 citations in OpenAlex.
- Photoreceptor replacement: a disease-agnostic approach for the treatment of advanced retinal degeneration.Eye (London, England) · 2026Review
- Lipid nanoparticles enable mRNA delivery to diverse cell types of the inner Retina.Molecular therapy. Nucleic acids · 2026Article
- Minocycline and bone marrow-derived mononuclear cells as potential therapeutics for hereditary retinal degenerations.Acta ophthalmologica · 2026Article
- CCR1 signaling as a common injury pathway in retinal degeneration.Journal of neuroinflammation · 2026Article
- Single-cell analysis reveals impaired Müller glia-mediated intercellular communication and photoreceptor pathology in USH1C retinal organoids.Cellular and molecular life sciences : CMLS · 2026Article
- Aberrant retinal structure and vasculature in mouse models of dominant retinopathies caused by CRX homeodomain mutations.Scientific reports · 2026Article
- Microglia maintain retinal redox homeostasis following ablation of rod photoreceptors in zebrafish.The Journal of biological chemistry · 2026Article
- Transplantation of human stem cell-derived cone photoreceptors partially restores vision in aged rd1 mice with advanced retinal degeneration.Stem cells (Dayton, Ohio) · 2026Article
- Eyedrop Administration of DPP-4 Inhibitors: A New Strategy for Treating Early Stages of Diabetic Retinal Disease.International journal of molecular sciences · 2026Review
- In vivo elastography of the human retina using light-evoked intrinsic actuation.bioRxiv : the preprint server for biology · 2026Article
- Aberrant retinal structure and vasculature in mouse models of dominant retinopathies caused bybioRxiv : the preprint server for biology · 2026Article
- Pre-existing retinal inflammation exacerbates gene therapy-associated uveitis in more rapidly progressive retinal degeneration.Molecular therapy. Advances · 2026Article
- The pathogenesis of müller cell glial-mesenchymal transition in retinal fibrosis-related eye diseases.Frontiers in cell and developmental biology · 2026Review
- Article
- Eight-year follow-up of phenotypic progression in a Chinese XLRP pedigree with a novelFrontiers in genetics · 2026Article
- Optogenetic vision restoration in the face of secondary and tertiary remodeling in the rd1 mouse retina.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Effect of degeneration stage on non-viral tissue transfection ofMolecular therapy. Nucleic acids · 2025Article
- Autophagy Regulates Müller Glial Cell Inflammatory Activation.Investigative ophthalmology & visual science · 2025Article
- Dysregulation of Mitochondrial Iron Regulators as a Basis of Iron-Mediated Retinal Degeneration in Rats.Neurotoxicity research · 2025Article
- A Hydrogel-Based Multiplex Coculture Platform for Retinal Component Cells.ACS applied bio materials · 2025Article
36 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Despite different aetiologies, most inherited retinal disorders culminate in photoreceptor loss, which induces concomitant changes in the neural retina, one of the most striking being reactive gliosis by Müller cells. It is typically assumed that photoreceptor loss leads to an upregulation of glial fibrilliary acidic protein (Gfap) and other intermediate filament proteins, together with other gliosis-related changes, including loss of integrity of the outer limiting membrane (OLM) and deposition of proteoglycans. However, this is based on a mix of both injury-induced and genetic causes of photoreceptor loss. There are very few longitudinal studies of gliosis in the retina and none comparing these changes across models over time. Here, we present a comprehensive spatiotemporal assessment of features of gliosis in the degenerating murine retina that involves Müller glia. Specifically, we assessed Gfap, vimentin and chondroitin sulphate proteoglycan (CSPG) levels and outer limiting membrane (OLM) integrity over time in four murine models of inherited photoreceptor degeneration that encompass a range of disease severities (Crb1rd8/rd8, Prph2+/Δ307, Rho-/-, Pde6brd1/rd1). These features underwent very different changes, depending upon the disease-causing mutation, and that these changes are not correlated with disease severity. Intermediate filament expression did indeed increase with disease progression in Crb1rd8/rd8 and Prph2+/Δ307, but decreased in the Prph2+/Δ307 and Pde6brd1/rd1 models. CSPG deposition usually, but not always, followed the trends in intermediate filament expression. The OLM adherens junctions underwent significant remodelling in all models, but with differences in the composition of the resulting junctions; in Rho-/- mice, the adherens junctions maintained the typical rod-Müller glia interactions, while in the Pde6brd1/rd1 model they formed predominantly between Müller cells in late stage of degeneration. Together, these results show that gliosis and its associated processes are variable and disease-dependent.
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