ArticleExperimental neurology2023
Patterns of NFkB activation resulting from damage, reactive microglia, cytokines, and growth factors in the mouse retina.
Article in Experimental neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Environmental Exposures and Oxidative Stress in Retinal and Optic Nerve Diseases: Mechanisms, Consequences, and Therapeutic Opportunities.Antioxidants (Basel, Switzerland) · 2026Review
- 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
- Forced exercise modulates retinal inflammatory response and regulates miRNA expression to promote retinal neuroprotection during degeneration.bioRxiv : the preprint server for biology · 2025Article
- The neuroimmune interface in retinal regeneration.Progress in retinal and eye research · 2025Review
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- 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
- Experimental Framework for Assessing Mouse Retinal Regeneration Through Single-Cell RNA-Sequencing.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Review
- Induction, amplification, and propagation of diabetic retinopathy-associated inflammatory cytokines between human retinal microvascular endothelial and Müller cells and in the mouse retina.Cellular signalling · 2024Article
- Monocyte Invasion into the Retina Restricts the Regeneration of Neurons from Müller Glia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Neuroinflammation as a cause of differential Müller cell regenerative responses to retinal injury.Science advances · 2024Article
- Article
- Crosstalk Between Microglia and Müller Glia in the Age-Related Macular Degeneration: Role and Therapeutic Value of Neuroinflammation.Aging and disease · 2024Review
- 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
- Apnea of prematurity induces short and long-term development-related transcriptional changes in the murine cerebellum.Current research in neurobiology · 2023Article
- Modeling inducible neuropathologies of the retina with differential phenotypes in organoids.Frontiers in cellular neuroscience · 2023Article
- Genetic and epigenetic regulators of retinal Müller glial cell reprogramming.Advances in ophthalmology practice and researchReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Müller glia are a cellular source for neuronal regeneration in vertebrate retinas. However, the capacity for retinal regeneration varies widely across species. Understanding the mechanisms that regulate the reprogramming of Müller glia into progenitor cells is key to reversing the loss of vision that occurs with retinal diseases. In the mammalian retina, NFkB signaling promotes glial reactivity and represses the reprogramming of Müller glia into progenitor cells. Here we investigate different cytokines, growth factors, cell signaling pathways, and damage paradigms that influence NFkB-signaling in the mouse retina. We find that exogenous TNF and IL1β potently activate NFkB-signaling in Müller glia in undamaged retinas, and this activation is independent of microglia. By comparison, TLR1/2 agonist indirectly activates NFkB-signaling in Müller glia, and this activation depends on the presence of microglia as Tlr2 is predominantly expressed by microglia, but not other types of retinal cells. Exogenous FGF2 did not activate NFkB-signaling, whereas CNTF, Osteopontin, WNT4, or inhibition of GSK3β activated NFkB in Müller glia in the absence of neuronal damage. By comparison, dexamethasone, a glucocorticoid agonist, suppressed NFkB-signaling in Müller glia in damaged retinas, in addition to reducing numbers of dying cells and the accumulation of reactive microglia. Although NMDA-induced retinal damage activated NFkB in Müller glia, optic nerve crush had no effect on NFkB activation within the retina, whereas glial cells within the optic nerve were responsive. We conclude that the NFkB pathway is activated in retinal Müller glia in response to many different cell signaling pathways, and activation often depends on signals produced by reactive microglia.
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Registered trials
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