ArticleNeuroscience bulletin2020
SOCS3 Attenuates GM-CSF/IFN-γ-Mediated Inflammation During Spontaneous Spinal Cord Regeneration.
Article in Neuroscience bulletin, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- LIF and Oncostatin M mitigate LPS-induced acute endometritis via distinct immunoregulatory mechanisms in peritoneal macrophagesiScience · 2026Article
- Tibolone Improves Motor Recovery and Regulates Neuroinflammation and Gliosis in a Model of Traumatic Spinal Cord Injury.International journal of molecular sciences · 2025Article
- GM-CSF Promotes the Development of Dysfunctional Vascular Networks in Moyamoya Disease.Neuroscience bulletin · 2024Article
- Stat3 Has a Different Role in Axon Growth During Development Than It Does in Axon Regeneration After Injury.Molecular neurobiology · 2024Article
- Article
- Electrical stimulation with polypyrrole-coated polycaprolactone/silk fibroin scaffold promotes sacral nerve regeneration by modulating macrophage polarisation.Biomaterials translational · 2024Article
- Identification of key genes increasing susceptibility to atrial fibrillation in nonalcoholic fatty liver disease and the potential mechanisms: mitochondrial dysfunction and systemic inflammation.Frontiers in pharmacology · 2024Article
- Enterovirus D68 infection upregulates SOCS3 expression to inhibit JAK-STAT3 signaling and antagonize the innate interferon response of the host.Virologica Sinica · 2023Article
- Heat shock factor 1 promotes neurite outgrowth and suppresses inflammation in the severed spinal cord of geckos.Neural regeneration research · 2023Article
- Ruxolitinib attenuates secondary injury after traumatic spinal cord injury.Neural regeneration research · 2022Article
- Identifying Rare Genetic Variants of Immune Mediators as Risk Factors for Autism Spectrum Disorder.Genes · 2022Article
- Metabolomic analysis of vascular cognitive impairment due to hepatocellular carcinoma.Frontiers in neurology · 2022Article
- Neuroinflammation in retinitis pigmentosa: Therapies targeting the innate immune system.Frontiers in immunology · 2022Review
- Inflammation after spinal cord injury: a review of the critical timeline of signaling cues and cellular infiltration.Journal of neuroinflammation · 2021Review
- Self-Control of Inflammation during Tail Regeneration of Lizards.Journal of developmental biology · 2021Review
- Adult astrocytes from reptiles are resistant to proinflammatory activation via sustaining Vav1 expression.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SOCS3, a feedback inhibitor of the JAK/STAT signal pathway, negatively regulates axonal regrowth and inflammation in the central nervous system (CNS). Here, we demonstrated a distinct role of SOCS3 in the injured spinal cord of the gecko following tail amputation. Severing the gecko spinal cord did not evoke an inflammatory cascade except for an injury-stimulated elevation of the granulocyte/macrophage colony-stimulating factor (GM-CSF) and interferon gamma (IFN-γ) cytokines. Simultaneously, the expression of SOCS3 was upregulated in microglia, and unexpectedly not in neurons. Enforced expression of SOCS3 was sufficient to suppress the GM-CSF/IFN-γ-driven inflammatory responses through its KIR domain by attenuating the activities of JAK1 and JAK2. SOCS3 was also linked to GM-CSF/IFN-γ-induced cross-tolerance. Transfection of adenovirus overexpressing SOCS3 in the injured cord resulted in a significant decrease of inflammatory cytokines. These results reveal a distinct role of SOCS3 in the regenerating spinal cord, and provide new hints for CNS repair in mammals.
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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 OpenQuestion graph.