ArticleCell reports methods2022
A genetic tool for the longitudinal study of a subset of post-inflammatory reactive astrocytes.
Article in Cell reports methods, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Innate immune signaling and functions in astrocytes.Nature immunology · 2026Review
- A human telomerase reverse transcriptase-derived peptide GV1001 rescues neurodegeneration in a mouse model of Alzheimer disease.Experimental & molecular medicine · 2026Article
- The regulatory code of injury-responsive enhancers enables precision cell-state targeting in the CNS.Nature neuroscience · 2026Article
- Article
- Review
- Aryl hydrocarbon receptor deficiency enhances astrocyte sensitivity to LPS-induced inflammation.Frontiers in cellular neuroscience · 2025Article
- Adenosine triggers early astrocyte reactivity that provokes microglial responses and drives the pathogenesis of sepsis-associated encephalopathy in mice.Nature communications · 2024Article
- An adhesion signaling axis involving Dystroglycan, β1-Integrin, and Cas adaptor proteins regulates the establishment of the cortical glial scaffold.PLoS biology · 2023Article
- Functional roles of reactive astrocytes in neuroinflammation and neurodegeneration.Nature reviews. Neurology · 2023Review
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Authors and funding
9 authors.
Funding
Abstract
Astrocytes are vital support cells that ensure proper brain function. In brain disease, astrocytes reprogram into a reactive state that alters many of their cellular roles. A long-standing question in the field is whether downregulation of reactive astrocyte (RA) markers during resolution of inflammation is because these astrocytes revert back to a non-reactive state or die and are replaced. This has proven difficult to answer mainly because existing genetic tools cannot distinguish between healthy versus RAs. Here we describe the generation of an inducible genetic tool that can be used to specifically target and label a subset of RAs. Longitudinal analysis of an acute inflammation model using this tool revealed that the previously observed downregulation of RA markers after inflammation is likely due to changes in gene expression and not because of cell death. Our findings suggest that cellular changes associated with astrogliosis after acute inflammation are largely reversible.
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Registered trials
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