ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2019
White Matter Stroke Induces a Unique Oligo-Astrocyte Niche That Inhibits Recovery.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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Who cites it
33 citing papers in PubMed, 43 citations in OpenAlex.
- Neuroimmune-oligovascular signaling shapes oligodendrocyte precursor cell fate and repair after ischemic stroke.Cell communication and signaling : CCS · 2026Review
- Multiscale Mechanisms that Underlie Intermittent Theta-burst Stimulation in Post-stroke Motor Recovery: From Molecular Signaling to Network Reorganization.Translational stroke research · 2026Review
- Inhibition of SLC11A1-Mediated Lysosomal Iron Accumulation in Microglia Promotes Repair Following White Matter Stroke.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- White matter injury after brain ischemia.Experimental neurology · 2026Review
- Targeting angiogenesis and white matter repair for enhanced functional recovery after acute ischemic stroke: A focus on the roles of glial cells.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Breast milk stem cells integrate into cellular remodeling and functional differentiation in the ischemic brain.Scientific reports · 2025Article
- Article
- Experimental Ischemic Stroke Induces Secondary Bihemispheric White Matter Degeneration and Long-Term Cognitive Impairment.Translational stroke research · 2025Article
- Changing genes, cells and networks to reprogram the brain after stroke.Nature neuroscience · 2025Review
- Characterisation of GPR17-expressing oligodendrocyte precursors in human ischaemic lesions and correlation with reactive glial responses.The Journal of pathology · 2025Article
- Reactive Astrocytes and Emerging Roles in Central Nervous System (CNS) Disorders.Cold Spring Harbor perspectives in biology · 2024Review
- YTHDF2-regulated matrilin-3 mitigates post-reperfusion hemorrhagic transformation in ischemic stroke via the PI3K/AKT pathway.Journal of neuropathology and experimental neurology · 2024Article
- PRMT5 inhibition shows in vitro efficacy against H3K27M-altered diffuse midline glioma, but does not extend survival in vivo.Scientific reports · 2024Article
- Cerebrovascular disease is associated with Alzheimer's plasma biomarker concentrations in adults with Down syndrome.Brain communications · 2024Article
- Motor Activity-Induced White Matter Repair in White Matter Stroke.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Oligodendrocyte progenitor cells in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2023Review
- Role of Crosstalk between Glial Cells and Immune Cells in Blood-Brain Barrier Damage and Protection after Acute Ischemic Stroke.Aging and disease · 2023Review
- Decoding the molecular crosstalk between grafted stem cells and the stroke-injured brain.Cell reports · 2023Article
- Roles of NG2 Glia in Cerebral Small Vessel Disease.Neuroscience bulletin · 2023Review
- Neuroprotective astroglial response to neural damage and its relevance to affective disorders.Exploration of neuroprotective therapy · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Subcortical white matter stroke is a common stroke subtype. White matter stroke stimulates adjacent oligodendrocyte progenitor cells (OPCs) to divide and migrate to the lesion, but stroke OPCs have only a limited differentiation into mature oligodendrocytes. To understand the molecular systems that are active in OPC responses in white matter stroke, OPCs were virally labeled and laser-captured in the region of partial damage adjacent to the infarct in male mice. RNAseq indicates two distinct OPC transcriptomes associated with the proliferative and limited-regeneration phases of OPCs after stroke. Molecular pathways related to nuclear receptor activation, ECM turnover, and lipid biosynthesis are activated during proliferative OPC phases after stroke; inflammatory and growth factor signaling is activated in the later stage of limited OPC differentiation. Within ECM proteins, Matrilin-2 is induced early after stroke and then rapidly downregulated. Prediction of upstream regulators of the OPC stroke transcriptome identifies several candidate molecules, including Inhibin A-a negative regulator of Matrilin-2. Inhibin A is induced in reactive astrocytes after stroke, including in humans. In functional assays, Matrilin-2 induces OPC differentiation, and Inhibin A inhibits OPC Matrilin-2 expression and inhibits OPC differentiation.
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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.