ArticleJournal of neuroinflammation2019
All trans-retinoic acid protects against acute ischemic stroke by modulating neutrophil functions through STAT1 signaling.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 89 citations in OpenAlex.
- Type I IFN dynamics orchestrate protective ICAM1iScience · 2026Article
- Review
- Evolution of neutrophil extracellular traps in the pathology of stroke.Neural regeneration research · 2026Article
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- Correlation of composite inflammatory indices and homocysteine with the severity of acute ischemic stroke: A retrospective study.Medicine · 2026Article
- Tudor domain-containing protein 9-targeting siRNA nanoparticles alleviate Pseudomonas aeruginosa lung injury in preclinical models by promoting neutrophil cuproptosis.Nature communications · 2026Article
- An NRIP1-Centric Monocyte Immunogenetic Bridge Between Heart Failure and Ischemic Stroke.Journal of inflammation research · 2026Article
- Discovery of a novel Nrf2 activator that modulates mitochondrial function in neurons by regulating DHRS3-Nrf2 interaction after ischemic stroke.Theranostics · 2026Article
- Neuromelanin-induced cellular stress and neurotoxicity in the pathogenesis of Parkinson's disease.Apoptosis : an international journal on programmed cell death · 2025Review
- Article
- atRA Attenuates High Salt-Driven EAE Mainly Through Suppressing Th17-Like Regulatory T Cell Response Mediated by the Inhibition of IL-23R Signaling Pathway.Inflammation · 2025Article
- The emerging role of neutrophil extracellular traps in autoimmune and autoinflammatory diseases.MedComm · 2025Review
- Article
- Unveiling the power of Treg.Sig: a novel machine-learning derived signature for predicting ICI response in melanoma.Frontiers in immunology · 2025Article
- STAT signaling pathways in immune cells and their associated mechanisms in cancer pathogenesis.BioImpacts : BI · 2025Review
- STING Activation in Macrophages and Microglia Drives Poststroke Inflammation: Implications for Neuroinflammatory Mechanisms and Therapeutic Interventions.CNS neuroscience & therapeutics · 2024Article
- All-trans retinoic acid inhibits glioblastoma progression and attenuates radiation-induced brain injury.JCI insight · 2024Article
- Neuroprotective effects of all-trans-retinoic acid are mediated via downregulation of TLR4/NF-κB signaling in a rat model of middle cerebral artery occlusion.Neurosciences (Riyadh, Saudi Arabia) · 2024Article
- Permissive lung neutrophils facilitate tuberculosis immunopathogenesis in male phagocyte NADPH oxidase-deficient mice.PLoS pathogens · 2024Article
- Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
background and purposeRegulation of neural inflammation is considered as a vital therapeutic target in ischemic stroke. All-trans retinoic acid (atRA), a potent immune modulator, has raised interest in the field of stroke therapy. However, the immunological mechanisms for atRA-mediated neuroprotection remain elusive. The current study evaluated the impact of atRA on post-stroke neural inflammation and elucidated the mechanisms involved in the regulation of related neutrophil functions.
methodsatRA was prophylactically administered to mice 1 day before transient middle cerebral artery occlusion (tMCAO, 1 h) and repeated daily immediately after reperfusion for 3 days. Stroke outcomes, neutrophil polarization, and formation of neutrophil extracellular traps (NETs) in the stroke lesion were assessed. Neutrophil depletion was induced with anti-Ly6G antibodies. Primary neutrophil cultures were used to explore the mechanisms of atRA treatment.
resultsProphylactic atRA treatment reduced infarct volumes and neurological deficits at 1 day after tMCAO. Post-stroke neural inflammation was attenuated and neutrophil accumulation in lesion was downregulated. atRA treatment skewed neutrophil toward N2 phenotype which facilitated its clearance by macrophage and inhibited NETs formation. The functions of neutrophil were indispensable in the protective effects of atRA and were associated with suppression to STAT1 signaling by atRA. Administration of atRA after stroke still provided efficient protection to cerebral ischemia.
conclusionatRA displays potent therapeutic efficacy in ischemic stroke by attenuating neural inflammation. Treatment of atRA impeded neutrophil accumulation, favored N2 polarization, and forbade NETs formation in ischemic lesion. STAT1 signaling played a decisive role in the mechanisms of atRA-afforded regulation to neutrophil.
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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 Socratic graph.