ArticleThe Journal of clinical investigation2019
Nuclear factor I-A regulates diverse reactive astrocyte responses after CNS injury.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Critical role of high-dose Astragalus in Buyang Huanwu Decoction for enhancing neurovascular coupling in a Qi Deficiency and Blood Stasis animal model.Chinese medicine · 2026Article
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- Neocortical tau propagation is a mediator of clinical heterogeneity in Alzheimer's disease.Molecular psychiatry · 2025Article
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- Astrocyte-derived extracellular vesicular NFIA mediates obesity-associated cognitive impairment.Journal of neuroinflammation · 2025Article
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- Enhancer Dynamics and Spatial Organization Drive Anatomically Restricted Cellular States in the Human Spinal Cord.bioRxiv : the preprint server for biology · 2025Article
- Identification of a Subpopulation of Astrocyte Progenitor Cells in the Neonatal Subventricular Zone: Evidence that Migration is Regulated by Glutamate Signaling.Neurochemical research · 2025Article
- Generating iAstrocytes From Human Induced Pluripotent Stem Cells by Combining Low-Density Passaging of Neural Progenitor Cells and Transcription Factor NFIA Transdifferentiation.Current protocols · 2024Article
- Brain repair mechanisms after cell therapy for stroke.Brain : a journal of neurology · 2024Review
- Astrocytic Slc4a4 regulates blood-brain barrier integrity in healthy and stroke brains via a CCL2-CCR2 pathway and NO dysregulation.Cell reports · 2024Article
- Cell-specific NFIA upregulation promotes epileptogenesis by TRPV4-mediated astrocyte reactivity.Journal of neuroinflammation · 2023Article
- Subventricular zone cytogenesis provides trophic support for neural repair in a mouse model of stroke.Nature communications · 2023Article
- Article
- Human Alzheimer's disease reactive astrocytes exhibit a loss of homeostastic gene expression.Acta neuropathologica communications · 2023Article
- Role of hyperbaric oxygen therapy in PDGF-BB-mediated astrogliosis in traumatic brain injury rats associated with ERK1/2 signaling pathway inhibition.European journal of medical research · 2023Article
- Transplantation of A2 type astrocytes promotes neural repair and remyelination after spinal cord injury.Cell communication and signaling : CCS · 2023Article
- Exposure to war and conflict: The individual and inherited epigenetic effects on health, with a focus on post-traumatic stress disorder.Frontiers in epidemiology · 2023Review
- Astrocyte contribution to dysfunction, risk and progression in neurodegenerative disorders.Nature reviews. Neuroscience · 2023Review
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Authors and funding
13 authors.
Funding
Abstract
Reactive astrocytes are associated with every form of neurological injury. Despite their ubiquity, the molecular mechanisms controlling their production and diverse functions remain poorly defined. Because many features of astrocyte development are recapitulated in reactive astrocytes, we investigated the role of nuclear factor I-A (NFIA), a key transcriptional regulator of astrocyte development whose contributions to reactive astrocytes remain undefined. Here, we show that NFIA is highly expressed in reactive astrocytes in human neurological injury and identify unique roles across distinct injury states and regions of the CNS. In the spinal cord, after white matter injury (WMI), NFIA-deficient astrocytes exhibit defects in blood-brain barrier remodeling, which are correlated with the suppression of timely remyelination. In the cortex, after ischemic stroke, NFIA is required for the production of reactive astrocytes from the subventricular zone (SVZ). Mechanistically, NFIA directly regulates the expression of thrombospondin 4 (Thbs4) in the SVZ, revealing a key transcriptional node regulating reactive astrogenesis. Together, these studies uncover critical roles for NFIA in reactive astrocytes and illustrate how region- and injury-specific factors dictate the spectrum of reactive astrocyte responses.
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