ArticleGlia2022
NFkB-signaling promotes glial reactivity and suppresses Müller glia-mediated neuron regeneration in the mammalian retina.
Article in Glia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 82 citations in OpenAlex.
- Beneficial effects of dietary green tea extract supplementation during necrotic enteritis challenge in broiler chicks.Poultry science · 2026Article
- Microglia maintain retinal redox homeostasis following ablation of rod photoreceptors in zebrafish.The Journal of biological chemistry · 2026Article
- FGF Signaling Potentiates Müller Glia for Mammalian Retinal Regeneration.bioRxiv : the preprint server for biology · 2026Article
- Transient YAP activation uncovers the neurogenic potential of proliferative mammalian Müller glia.PNAS nexus · 2026Article
- Lipoxin B4 Mitigates TRPV4-Activated Müller Cell Gliosis During Ocular Hypertension.Investigative ophthalmology & visual science · 2026Article
- Tumor Necrosis Factor Alpha-Mediated Interaction Between Microglia and Müller Cells Exacerbates Retinal Ganglion Cell Damage in Experimental Glaucoma.Neuroscience bulletin · 2026Article
- Sphingosine-1-Phosphate Signaling through Müller Glia Regulates Neuroprotection, Accumulation of Immune Cells, and Neuronal Regeneration in the Rodent Retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Lipoxin BbioRxiv : the preprint server for biology · 2025Article
- Ambra1 Deficiency Improves Retinal Inflammation in Streptozotocin-Induced Diabetic Mouse Models.Cureus · 2025Article
- Melatonin Synergises the Chemotherapeutic Effect of Temozolomide in Glioblastoma by Suppressing NF-κB/COX-2 Signalling Pathways.Journal of cellular and molecular medicine · 2025Article
- Depletion of Polypyrimidine tract binding protein 1 (ptbp1) activates Müller glia-derived proliferation during zebrafish retina regeneration via modulation of the senescence secretome.Experimental eye research · 2025Article
- Article
- The neuroimmune interface in retinal regeneration.Progress in retinal and eye research · 2025Review
- Latent epigenetic programs in Müller glia contribute to stress and disease response in the retina.Developmental cell · 2025Article
- Preserving blood-retinal barrier integrity: a path to retinal ganglion cell protection in glaucoma and traumatic optic neuropathy.Cell regeneration (London, England) · 2025Review
- Investigating Müller glia reprogramming in mice: a retrospective of the last decade, and a look to the future.Neural regeneration research · 2025Article
- Timing neural development and regeneration.Current opinion in neurobiology · 2025Review
- Article
- Article
- Sphingosine-1-phosphate signaling regulates the ability of Müller glia to become neurogenic, proliferating progenitor-like cells.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Müller glia (MG) in mammalian retinas are incapable of regenerating neurons after damage, whereas the MG in lower vertebrates regenerate functional neurons. Identification of cell signaling pathways and gene regulatory networks that regulate MG-mediated regeneration is key to harnessing the regenerative potential of MG. Here, we study how NFkB-signaling influences glial responses to damage and reprogramming of MG into neurons in the rodent retina. We find activation of NFkB and dynamic expression of NFkB-associated genes in MG after damage, however damage-induced NFkB activation is inhibited by microglia ablation. Knockout of NFkB in MG suppressed the accumulation of immune cells after damage. Inhibition of NFkB following NMDA-damage significantly enhanced the reprogramming of Ascl1-overexpressing MG into neuron-like cells. scRNA-seq of retinal glia following inhibition of NFkB reveals coordination with signaling via TGFβ2 and suppression of NFI and Id transcription factors. Inhibition of Smad3 signal transducer or Id transcription factors increased numbers of neuron-like cells produced by Ascl1-overexpressing MG. We conclude that NFkB is a key signaling hub that is activated in MG after damage, mediates the accumulation of immune cells, and suppresses the neurogenic potential of MG.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.