ArticleStroke and vascular neurology2022
Novel role of STAT3 in microglia-dependent neuroinflammation after experimental subarachnoid haemorrhage.
Article in Stroke and vascular neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Compartmental Cerebrospinal Fluid Events Occurring after Subarachnoid Hemorrhage: An "Heparin Oriented" Systematic Review.International journal of molecular sciences · 2023Pooled it
- Long-term clinical and biomarker observations following rituximab exposure in two siblings with CSF1R-related leukoencephalopathy: a preliminary familial case series.Communications medicine · 2026Article
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- Varicose projection astrocytes: Conserved reactive cells in brain pathology.Science advances · 2026Article
- Neuroglial Response to High-Amplitude, Short-Duration Pressure Transients in Monoculture.Cell biochemistry and function · 2026Article
- IL-10-STAT3-Dependent Transcriptional Regulation in Microglia: Alzheimer's Disease and Neuroinflammation.Biomedicines · 2026Review
- Microglial CX3CR1 deficiency regulates the selective vulnerability of cone photoreceptors via STAT3/CCL-ACKR1 signaling in the mouse retina.Experimental & molecular medicine · 2026Article
- Gut metabolite indole-3-acetic acid aggravates neuropsychiatric lupus via the AHR/STAT3 pathway in microglia.Communications biology · 2026Article
- Epidermal growth factor receptor modulation for neural repair: Implications for neurodegenerative disease therapy.Frontiers in molecular neuroscience · 2026Review
- Structure matters: commensalFrontiers in cellular neuroscience · 2026Article
- Network Pharmacology, Molecular Docking, andCurrent topics in medicinal chemistry · 2026Article
- Neuronal PARIS-STAT3 axis drives tau pathology and glial activation in Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- Identification of post-translational modification-related biomarkers in ischemic stroke using bioinformatics and machine learning.Scientific reports · 2025Article
- Identification of Key Ferroptosis-Related Genes as Potential Diagnostic Biomarkers for Ischemic Stroke: Evidences from Integrated Bioinformatics Analysis and Experiments.Cellular and molecular neurobiology · 2025Article
- Article
- Multi-Omics Approach Reveals Genes and Pathways Affected in Miller-Dieker Syndrome.Molecular neurobiology · 2025Article
- Long Noncoding RNA ISA1 Protects Against Ischemic Brain Damage by Promoting the Transformation of Microglia Toward Anti-inflammatory Phenotype via the SOCS3/JAK2/STAT3 Pathway.Neurochemical research · 2025Article
- Modulating Neuroinflammation as a Prospective Therapeutic Target in Alzheimer's Disease.Cells · 2025Review
- Mechanical ventilation amplifies intratracheal lipopolysaccharide-induced plasma and brainstem inflammation in preterm foetal sheep.Brain communications · 2025Article
- Identification of RN7SK LncRNA as a novel biomarker in Alzheimer's disease using bioinformatics and expression analysis.Scientific reports · 2024Article
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Authors and funding
7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
background and purposeSignal transducer and activator of transcription 3 (STAT3) may contribute to the proinflammation in the central nervous system diseases by modulating the microglial responses. Thus, this study was intended to investigate the effect of STAT3 on microglia-dependent neuroinflammation and functional outcome after experimental subarachnoid haemorrhage (SAH).
methodsThe SAH model was established by endovascular perforation in the mouse. Real-time PCR (RtPCR) and western blot were used to examine the dynamic STAT3 signalling pathway responses after SAH. To clarify the role of the STAT3 signalling pathway in the microglia-dependent neuroinflammation after SAH, the microglia-specific STAT3 knockout (KO) mice were generated by the Cre-LoxP system. The neurological functions were assessed by Catwalk and Morris water maze tests. Neuronal loss after SAH was determined by immunohistochemistry staining. Microglial polarisation status after STAT3 KO was then examined by RtPCR and immunofluorescence.
resultsThe STAT3 and Janus kinase-signal transducer 2 activated immediately with the upregulation and phosphorylation after SAH. Downstream factors and related mediators altered dynamically and accordingly. Microglial STAT3 deletion ameliorated the neurological impairment and alleviated the early neuronal loss after SAH. To investigate the underlying mechanism, we examined the microglial reaction after STAT3 KO. STAT3 deletion reversed the increase of microglia after SAH. Loss of STAT3 triggered the early morphological changes of microglia and primed microglia from M1 to M2 polarisation. Functionally, microglial STAT3 deletion suppressed the SAH-induced proinflammation and promoted the anti-inflammation in the early phase.
conclusionsSTAT3 is closely related to the microglial polarisation transition and modulation of microglia-dependent neuroinflammation. Microglial STAT3 deletion improved neurological function and neuronal survival probably through promoting M2 polarisation and anti-inflammatory responses after SAH. STAT3 may serve as a promising therapeutic target to alleviate early brain injury after SAH.
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