ArticleScientific reports2017
Retinal cell death dependent reactive proliferative gliosis in the mouse retina.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 38 citations in OpenAlex.
- Reprogramming Glial Cell Metabolism via a tRNA Fragment Preserves Vision in Retinal Neurodegeneration.MedComm · 2026Article
- FGF Signaling Potentiates Müller Glia for Mammalian Retinal Regeneration.bioRxiv : the preprint server for biology · 2026Article
- In vivo and ex vivo evaluation of the responses of rat Müller glia after injury.Scientific reports · 2026Article
- The pathogenesis of müller cell glial-mesenchymal transition in retinal fibrosis-related eye diseases.Frontiers in cell and developmental biology · 2026Review
- Differential effects of HDAC inhibitors in the RhoCell death discovery · 2025Article
- Sustained EGFR Signaling Expands Otx2Cells · 2025Article
- Neuroinflammation as a cause of differential Müller cell regenerative responses to retinal injury.Science advances · 2024Article
- Combination of blockade of endothelin signalling and compensation of IGF1 expression protects the retina from degeneration.Cellular and molecular life sciences : CMLS · 2024Article
- Article
- Characterization of Macroglia Response during Tissue Repair in a Laser-Induced Model of Retinal Degeneration.International journal of molecular sciences · 2023Article
- Reliability of human retina organoid generation from hiPSC-derived neuroepithelial cysts.Frontiers in cellular neuroscience · 2023Article
- Modeling inducible neuropathologies of the retina with differential phenotypes in organoids.Frontiers in cellular neuroscience · 2023Article
- Cell Sources for Retinal Regeneration: Implication for Data Translation in Biomedicine of the Eye.Cells · 2022Review
- Early manifestations and differential gene expression associated with photoreceptor degeneration in Prom1-deficient retina.Disease models & mechanisms · 2021Article
- The TGFβ/Notch axis facilitates Müller cell-to-epithelial transition to ultimately form a chronic glial scar.Molecular neurodegeneration · 2021Article
- Stimulation of α7 nAChR leads to regeneration of damaged neurons in adult mammalian retinal disease models.Experimental eye research · 2021Article
- Diabetic retinal neurodegeneration as a form of diabetic retinopathy.International ophthalmology · 2021Review
- Alterations of retinal thickness measured by optical coherence tomography correlate with neurophysiological measures in diabetic polyneuropathy.Journal of diabetes investigation · 2021Article
- Mouse Retinal Organoid Growth and Maintenance in Longer-Term Culture.Frontiers in cell and developmental biology · 2021Article
- Visual Outcomes in Experimental Rodent Models of Blast-Mediated Traumatic Brain Injury.Frontiers in molecular neuroscience · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegeneration is a common starting point of reactive gliosis, which may have beneficial and detrimental consequences. It remains incompletely understood how distinctive pathologies and cell death processes differentially regulate glial responses. Müller glia (MG) in the retina are a prime model: Neurons are regenerated in some species, but in mammals there may be proliferative disorders and scarring. Here, we investigated the relationship between retinal damage and MG proliferation, which are both induced in a reproducible and temporal order in organotypic culture of EGF-treated mouse retina: Hypothermia pretreatment during eye dissection reduced neuronal cell death and MG proliferation; stab wounds increased both. Combined (but not separate) application of defined cell death signaling pathway inhibitors diminished neuronal cell death and maintained MG mitotically quiescent. The level of neuronal cell death determined MG activity, indicated by extracellular signal-regulated kinase (ERK) phosphorylation, and proliferation, both of which were abolished by EGFR inhibition. Our data suggest that retinal cell death, possibly either by programmed apoptosis or necrosis, primes MG to be able to transduce the EGFR-ERK activity required for cell proliferation. These results imply that cell death signaling pathways are potential targets for future therapies to prevent the proliferative gliosis frequently associated with certain neurodegenerative conditions.
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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.