ArticleExperimental neurology2015
Activation of glucocorticoid receptors in Müller glia is protective to retinal neurons and suppresses microglial reactivity.
Article in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Molecular mechanisms of excitotoxicity and their relevance to the pathogenesis of neurodegenerative diseases-an update.Acta pharmacologica Sinica · 2025Review
- Review
- Glucocorticoid-Dependent Retinal Degeneration and Vision Impairment in Mice Susceptible to Prenatal Stress-Induced Behavioral Abnormalities.Cellular and molecular neurobiology · 2024Article
- Timed topical dexamethasone eye drops improve mitochondrial function to prevent severe retinopathy of prematurity.Angiogenesis · 2024Article
- Timed topical dexamethasone eye drops improve mitochondrial function to prevent severe retinopathy of prematurity.Research square · 2024Article
- Useful Role of a New Generation of Dexamethasone, Vitamin E and Human Serum Albumin Microparticles in the Prevention of Excitotoxicity Injury in Retinal Ocular Diseases.Pharmaceutics · 2024Article
- The glucocorticoid receptor as a master regulator of the Müller cell response to diabetic conditions in mice.Journal of neuroinflammation · 2024Article
- Inflammation is a critical factor for successful regeneration of the adult zebrafish retina in response to diffuse light lesion.Frontiers in cell and developmental biology · 2024Article
- The Disorganization of Retinal Inner Layers Is Correlated to Müller Cells Impairment in Diabetic Macular Edema: An Imaging and Omics Study.International journal of molecular sciences · 2023Observational
- Yigan Mingmu Decoction inhibits diabetic macular edema through regulating Kir4.1/AQP4 axis: a study based on network pharmacology.American journal of translational research · 2023Article
- Patterns of NFkB activation resulting from damage, reactive microglia, cytokines, and growth factors in the mouse retina.Experimental neurology · 2023Article
- Retinal ganglion cell survival after severe optic nerve injury is modulated by crosstalk between Jak/Stat signaling and innate immune responses in the zebrafish retina.Development (Cambridge, England) · 2022Article
- Molecular regulation of neuroinflammation in glaucoma: Current knowledge and the ongoing search for new treatment targets.Progress in retinal and eye research · 2022Review
- Article
- Article
- Müller Glia-Mediated Retinal Regeneration.Molecular neurobiology · 2021Review
- Article
- The role of Müller cell glucocorticoid signaling in diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2020Review
- Matrix-metalloproteinase expression and gelatinase activity in the avian retina and their influence on Müller glia proliferation.Experimental neurology · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Reactive microglia and macrophages are prevalent in damaged retinas. Glucocorticoid signaling is known to suppress inflammation and the reactivity of microglia and macrophages. In the vertebrate retina, the glucocorticoid receptor (GCR) is known to be activated and localized to the nuclei of Müller glia (Gallina et al., 2014). Accordingly, we investigated how signaling through GCR influences the survival of neurons using the chick retina in vivo as a model system. We applied intraocular injections of GCR agonist or antagonist, assessed microglial reactivity, and the survival of retinal neurons following different damage paradigms. Microglial reactivity was increased in retinas from eyes that were injected with vehicle, and this reactivity was decreased by GCR-agonist dexamethasone (Dex) and increased by GCR-antagonist RU486. We found that activation of GCR suppresses the reactivity of microglia and inhibited the loss of retinal neurons resulting from excitotoxicity. We provide evidence that the protection-promoting effects of Dex were maintained when the microglia were selectively ablated. Similarly, intraocular injections of Dex protected ganglion cells from colchicine-treatment and protected photoreceptors from damage caused by retinal detachment. We conclude that activation of GCR promotes the survival of ganglion cells in colchicine-damaged retinas, promotes the survival of amacrine and bipolar cells in excitotoxin-damaged retinas, and promotes the survival of photoreceptors in detached retinas. We propose that suppression of microglial reactivity is secondary to activation of GCR in Müller glia, and this mode of signaling is an effective means to lessen the damage and vision loss resulting from different types of retinal damage.
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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.