ArticleGlia2020
Ischemic preconditioning induces cortical microglial proliferation and a transcriptomic program of robust cell cycle activation.
Article in Glia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Gq Signaling in Microglia Triggers Interferon Responses and Improves Outcome After Ischemic Stroke.Glia · 2026Article
- High-altitude hypoxic cues and cerebral ischemic tolerance: an evidence-graded translational framework for stroke research.Frontiers in neuroscience · 2026Review
- Heterogeneity of Microglia in Ischemic Stroke from the Perspective of Single-Cell RNA Sequencing: Subset Characteristics, Mechanisms and Therapeutic Potential.Journal of central nervous system disease · 2026Review
- Localised delivery of interleukin-13 from a PLGA microparticle embedded GelMA hydrogel improves functional and histopathological recovery in a mouse contusion spinal cord injury model.Bioactive materials · 2025Article
- Physiological and injury-induced microglial dynamics across the lifespan.Cell reports · 2025Article
- Review
- The Role of Casr Inhibition-Mediated M2 Microglial Transformation in Ischemic Preconditioning Against Stroke.Current medical science · 2025Article
- Single-Cell RNA Sequencing Reveals Microglial Heterogeneity and Functional States After Cerebral Ischemia-Reperfusion Injury.Journal of inflammation research · 2025Article
- Brain Ischemic Tolerance Triggered by Preconditioning Involves Modulation of Tumor Necrosis Factor-α-Stimulated Gene 6 (TSG-6) in Mice Subjected to Transient Middle Cerebral Artery Occlusion.Current issues in molecular biology · 2024Article
- Microglial CMPK2 promotes neuroinflammation and brain injury after ischemic stroke.Cell reports. Medicine · 2024Article
- Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia.International journal of molecular sciences · 2024Review
- Impact of inflammatory preconditioning on murine microglial proteome response induced by focal ischemic brain injury.Frontiers in immunology · 2024Article
- Cortex-specific transcriptome profiling reveals upregulation of interferon-regulated genes after deeper cerebral hypoperfusion in mice.Frontiers in physiology · 2023Article
- Microglia dynamic response and phenotype heterogeneity in neural regeneration following hypoxic-ischemic brain injury.Frontiers in immunology · 2023Review
- A ferret brain slice model of oxygen-glucose deprivation captures regional responses to perinatal injury and treatment associated with specific microglial phenotypes.Bioengineering & translational medicine · 2022Article
- Article
- Ischemic Preconditioning Modulates the Peripheral Innate Immune System to Promote Anti-Inflammatory and Protective Responses in Mice Subjected to Focal Cerebral Ischemia.Frontiers in immunology · 2022Article
- Review
- A Subpopulation of Microglia Generated in the Adult Mouse Brain Originates from Prominin-1-Expressing Progenitors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Neuroprotective effects and mechanisms of ischemic/hypoxic preconditioning on neurological diseases.CNS neuroscience & therapeutics · 2021Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Ischemic preconditioning (IPC) is an experimental phenomenon in which a subthreshold ischemic insult applied to the brain reduces damage caused by a subsequent more severe ischemic episode. Identifying key molecular and cellular mediators of IPC will provide critical information needed to develop novel therapies for stroke. Here we report that the transcriptomic response of acutely isolated preconditioned cortical microglia is dominated by marked upregulation of genes involved in cell cycle activation and cellular proliferation. Notably, this transcriptional response occurs in the absence of cortical infarction. We employed ex vivo flow cytometry, immunofluorescent microscopy, and quantitative stereology methods on brain tissue to evaluate microglia proliferation following IPC. Using cellular colocalization of microglial (Iba1) and proliferation (Ki67 and BrdU) markers, we observed a localized increase in the number of microglia and proliferating microglia within the preconditioned hemicortex at 72, but not 24, hours post-IPC. Our quantification demonstrated that the IPC-induced increase in total microglia was due entirely to proliferation. Furthermore, microglia in the preconditioned hemisphere had altered morphology and increased soma volumes, indicative of an activated phenotype. Using transgenic mouse models with either fractalkine receptor (CX3CR1)-haploinsufficiency or systemic type I interferon signaling loss, we determined that microglial proliferation after IPC is dependent on fractalkine signaling but independent of type I interferon signaling. These findings suggest there are multiple distinct targetable signaling pathways in microglia, including CX3CR1-dependent proliferation that may be involved in IPC-mediated protection.
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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.