ArticleExperimental neurology2019
Matrix-metalloproteinase expression and gelatinase activity in the avian retina and their influence on Müller glia proliferation.
Article in Experimental neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Brillouin microscopic assessment of retinal stiffness during reactive Müller gliosis.Experimental eye research · 2026Article
- Ambra1 Deficiency Improves Retinal Inflammation in Streptozotocin-Induced Diabetic Mouse Models.Cureus · 2025Article
- Experimental Framework for Assessing Mouse Retinal Regeneration Through Single-Cell RNA-Sequencing.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Review
- Article
- Protein phosphatases regulate the formation of Müller glia-derived progenitor cells in the chick retina.Molecular and cellular neurosciences · 2024Article
- Retinal glia in myopia: current understanding and future directions.Frontiers in cell and developmental biology · 2024Review
- Protein phosphatases regulate the formation of Müller glia-derived progenitor cells in the chick retina.bioRxiv : the preprint server for biology · 2023Article
- Heparin-binding epidermal growth factor and fibroblast growth factor 2 rescue Müller glia-derived progenitor cell formation in microglia- and macrophage-ablated chick retinas.Development (Cambridge, England) · 2023Article
- Cell-Based Therapies: Strategies for Regeneration.Cold Spring Harbor perspectives in medicine · 2023Review
- Chromatin access regulates the formation of Müller glia-derived progenitor cells in the retina.Glia · 2023Article
- Modification of Müller Glial Cell Fate and Proliferation with the Use of Small Molecules.Advances in experimental medicine and biology · 2023Review
- Repopulated retinal microglia promote Müller glia reprogramming and preserve visual function in retinal degenerative mice.Theranostics · 2023Article
- Nuclear Factor I in neurons, glia and during the formation of Müller glia-derived progenitor cells in avian, porcine and primate retinas.The Journal of comparative neurology · 2022Article
- A comprehensive atlas of Aggrecan, Versican, Neurocan and Phosphacan expression across time in wildtype retina and in retinal degeneration.Scientific reports · 2022Article
- Fatty acid-binding proteins and fatty acid synthase influence glial reactivity and promote the formation of Müller glia-derived progenitor cells in the chick retina.Development (Cambridge, England) · 2022Article
- Matrix Metalloproteinases in Chemoresistance: Regulatory Roles, Molecular Interactions, and Potential Inhibitors.Journal of oncology · 2022Review
- Opicapone Protects Against Hyperhomocysteinemia-Induced Increase in Blood-Brain Barrier Permeability.Neurotoxicity research · 2021Article
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Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Gelatinases are a class of matrix metalloproteinases (MMPs) that degrade the extracellular matrix (ECM) to regulate intercellular signaling and cell migration. Gelatinase activity is tightly regulated via proteolytic activation and through the expression of tissue inhibitors of matrix metalloproteinases (TIMPs). Gelatinase activity has been implicated in retinal pathophysiology in different animal models and human disease. However, the role of gelatinases in retinal regeneration remains uncertain. In this study we investigated the dynamic changes in gelatinase activity in response to excitotoxic damage and how this enzymatic activity influenced the formation of Müller glia progenitor cells (MGPCs) in the avian retina. This study used hydrogels containing a gelatinase-degradable fluorescent peptide to measure gelatinase activity in vitro and dye quenched gelatin to localize enzymatic activity in situ. These data were corroborated by using single cell RNA sequencing (scRNA-seq). Gelatinase mRNA, specifically MMP2, was detected in oligodendrocytes and Non-Astrocytic Inner Retinal Glia (NIRG). Total retinal gelatinase activity was reduced following NMDA-treatment, and sustained inhibition of MMP2 prior to damage or growth factor treatment increased the formation of proliferating MGPCs and c-fos signaling. We observed that microglia, Müller glia (MG), and NIRG cells were involved in regulating changes in gelatinase activity through TIMP2 and TIMP3. Collectively, these findings implicate MMP2 in reprogramming of Muller glia into MGPCs.
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