ArticlePloS one2012
The reactivity, distribution and abundance of Non-astrocytic Inner Retinal Glial (NIRG) cells are regulated by microglia, acute damage, and IGF1.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed.
- The neuroimmune interface in retinal regeneration.Progress in retinal and eye research · 2025Review
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- Sphingosine-1-phosphate signaling regulates the ability of Müller glia to become neurogenic, proliferating progenitor-like cells.bioRxiv : the preprint server for biology · 2025Article
- Review
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- Protein phosphatases regulate the formation of Müller glia-derived progenitor cells in the chick retina.Molecular and cellular neurosciences · 2024Article
- 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
- Chromatin access regulates the formation of Müller glia-derived progenitor cells in the retina.Glia · 2023Article
- Cross-species cell-type assignment from single-cell RNA-seq data by a heterogeneous graph neural network.Genome research · 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
- 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
- Article
- Microglial Activation Is Associated With Vasoprotection in a Rat Model of Inflammatory Retinal Vasoregression.Frontiers in physiology · 2021Article
- The Contribution of Microglia to the Development and Maturation of the Visual System.Frontiers in cellular neuroscience · 2021Article
- NF-κB signaling regulates the formation of proliferating Müller glia-derived progenitor cells in the avian retina.Development (Cambridge, England) · 2020Article
- Tools and Approaches for Studying MicrogliaFrontiers in immunology · 2020Review
- Matrix-metalloproteinase expression and gelatinase activity in the avian retina and their influence on Müller glia proliferation.Experimental neurology · 2019Article
- Regenerative Effect of Growth Hormone (GH) in the Retina after Kainic Acid Excitotoxic Damage.International journal of molecular sciences · 2019Article
- Reactive microglia and IL1β/IL-1R1-signaling mediate neuroprotection in excitotoxin-damaged mouse retina.Journal of neuroinflammation · 2019Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Recent studies have described a novel type of glial cell that is scattered across the inner layers of the avian retina and possibly the retinas of primates. These cells have been termed Non-astrocytic Inner Retinal Glial (NIRG) cells. These cells are stimulated by insulin-like growth factor 1 (IGF1) to proliferate, migrate distally into the retina, and become reactive. These changes in glial activity correlate with increased susceptibility of retinal neurons and Müller glia to excitotoxic damage. The purpose of this study was to further study the NIRG cells in retinas treated with IGF1 or acute damage. In response to IGF1, the reactivity, proliferation and migration of NIRG cells persists through 3 days after treatment. At 7 days after treatment, the numbers and distribution of NIRG cells returns to normal, suggesting that homeostatic mechanisms are in place within the retina to maintain the numbers and distribution of these glial cells. By comparison, IGF1-induced microglial reactivity persists for at least 7 days after treatment. In damaged retinas, we find a transient accumulation of NIRG cells, which parallels the accumulation of reactive microglia, suggesting that the reactivity of NIRG cells and microglia are linked. When the microglia are selectively ablated by the combination of interleukin 6 and clodronate-liposomes, the NIRG cells down-regulate transitin and perish within the following week, suggesting that the survival and phenotype of NIRG cells are somehow linked to the microglia. We conclude that the abundance, reactivity and retinal distribution of NIRG cells can be dynamic, are regulated by homoestatic mechanisms and are tethered to the microglia.
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