ArticleMolecular therapy : the journal of the American Society of Gene Therapy2021
Microglial lnc-U90926 facilitates neutrophil infiltration in ischemic stroke via MDH2/CXCL2 axis.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 87 citations in OpenAlex.
- Unraveling competitive protein interactions: A critical step toward improved production and therapeutics.Journal of advanced research · 2026Review
- AAV Vector-Mediated Modulation of Signaling Pathways in Neurological Disorders: Insights From Cellular, Animal, and Human Studies.Cell biochemistry and function · 2026Review
- GPNMB modulates neutrophil extracellular trap formation: therapeutic implications for ischemic stroke.Journal of neuroinflammation · 2026Article
- PLAUR Exacerbates Neuroinflammation in Diabetic Ischemic Stroke by Driving Neutrophil-Mediated Blood-Brain Barrier Disruption and Reprogramming Microglial Metabolism.Neuromolecular medicine · 2026Article
- Neuroinflammation in Ischemic Stroke: Mechanisms, Systemic Interactions, and Therapeutic Targets.Translational stroke research · 2026Review
- Long noncoding RNA Nron and its functional motif modulate macrophage-mediated inflammatory response.Journal of advanced research · 2026Article
- Neuroinflammation after stroke: initiation, amplification and therapeutic prospects.Journal of translational medicine · 2026Review
- Targeting the interactions between neutrophils and microglia: a novel strategy for anti-inflammatory treatment of stroke.Acta pharmacologica Sinica · 2026Review
- Sustained Transcriptional Response to Lipopolysaccharide and Interleukin-4 in an Immortalized Mouse Microglial Cell Line.Molecular neurobiology · 2026Article
- Dynamic trajectories of inflammatory biomarkers and post-stroke cognitive impairment: a comprehensive review of neuroimmune mechanisms, longitudinal modeling, and clinical translation.Frontiers in neurology · 2026Review
- Cellular Communication Networks Mediated by Microglia in Ischemic Stroke.CNS neuroscience & therapeutics · 2025Review
- Single-cell transcriptomics of neuroinflammation and cerebrovascular endothelial cells in the aged rat hippocampus.iScience · 2025Article
- Immunological Mechanisms and Therapeutic Strategies in Cerebral Ischemia-Reperfusion Injury: From Inflammatory Response to Neurorepair.International journal of molecular sciences · 2025Review
- LncRNA-5829: a novel inhibitor of cardiac fibrosis.Cardiovascular diagnosis and therapy · 2025Article
- Neutrophil infiltration and microglial shifts in sepsis induced preterm brain injury: pathological insights.Acta neuropathologica communications · 2025Article
- Lactate accumulation from HIF-1α-mediated PMN-MDSC glycolysis restricts brain injury after acute hypoxia in neonates.Journal of neuroinflammation · 2025Article
- Review
- The role of inflammation in Ischemic stroke: from biomarker to treatment.Frontiers in immunology · 2025Review
- Noncanonical microprotein regulation of immunity.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- Body fluid multiomics in 3PM-guided ischemic stroke management: health risk assessment, targeted protection against health-to-disease transition, and cost-effective personalized approach are envisaged.The EPMA journal · 2024Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated long non-coding RNAs (lncRNAs) have been shown to contribute to the pathogenesis of ischemic stroke. However, the potential role of lncRNAs in post-stroke microglial activation remains largely unknown. Here, we uncovered that lncRNA-U90926 was significantly increased in microglia exposed to ischemia/reperfusion both in vivo and in vitro. In addition, adenovirus-associated virus (AAV)-mediated microglial U90926 silencing alleviated neurological deficits and reduced infarct volume in experimental stroke mice. Microglial U90926 knockdown could reduce the infiltration of neutrophils into ischemic lesion site, which might be attributed to the downregulation of C-X-C motif ligand 2 (CXCL2). Mechanistically, U90926 directly bound to malate dehydrogenase 2 (MDH2) and competitively inhibited the binding of MDH2 to the CXCL2 3' untranslated region (UTR), thus protecting against MDH2-mediated decay of CXCL2 mRNA. Taken together, our study demonstrated that microglial U90926 aggravated ischemic brain injury via facilitating neutrophil infiltration, suggesting that U90926 might be a potential biomarker and therapeutic target for ischemic stroke.
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