ArticleExperimental neurology2014
Expression of suppressor of cytokine signaling-3 (SOCS3) and its role in neuronal death after complete spinal cord injury.
Article in Experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 38 citations in OpenAlex.
- Electroacupuncture-modulated DHCR24 facilitates spinal cord injury recovery by attenuating apoptosis and neuroinflammation via the Wnt signaling pathway.Metabolic brain disease · 2026Article
- miR-19a-3p and miR-19b-3p Promote Microglia Activation Associated With Neuroinflammation.Journal of neuroscience research · 2026Article
- Overexpression of long non‑coding RNA H19 enhances cell viability and inhibits apoptosis in recurrent spontaneous abortion by targeting the miR-29a-3p/SOCS3 axis.In vitro cellular & developmental biology. Animal · 2025Article
- Single-Cell RNA Sequencing of the Primary Visual Cortex in Mice With Optic Nerve Injury.Investigative ophthalmology & visual science · 2025Article
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- Effect of 28 days treatment of baricitinib on mechanical allodynia, osteopenia, and loss of nerve fibers in an experimental model of type-1 diabetes mellitus.Pharmacological reports : PR · 2024Article
- Overexpression of BDNF Suppresses the Epileptiform Activity in Cortical Neurons of Heterozygous Mice with a Transcription Factor Sip1 Deletion.International journal of molecular sciences · 2024Article
- The Spatiotemporal Expression of SOCS3 in the Brainstem and Spinal Cord of Amyotrophic Lateral Sclerosis Mice.Brain sciences · 2024Article
- Review
- Targeting STAT3 Enzyme for Cancer Treatment.Mini reviews in medicinal chemistry · 2024Review
- Heat shock factor 1 promotes neurite outgrowth and suppresses inflammation in the severed spinal cord of geckos.Neural regeneration research · 2023Article
- Tofacitinib Promotes Functional Recovery after Spinal Cord Injury by Regulating Microglial Polarization via JAK/STAT Signaling Pathway.International journal of biological sciences · 2023Article
- Analysis of gene expression profiles in two spinal cord injury models.European journal of medical research · 2022Article
- Review
- Planet of the AAVs: The Spinal Cord Injury Episode.Biomedicines · 2021Review
- Total flavonoids of hawthorn leaves promote motor function recovery via inhibition of apoptosis after spinal cord injury.Neural regeneration research · 2021Article
- hsa-MiR-19a-3p and hsa-MiR-19b-3p Are Associated with Spinal Cord Injury-Induced Neuropathic Pain: Findings from a Genome-Wide MicroRNA Expression Profiling Screen.Neurotrauma reports · 2021Article
- SOCS3 Attenuates GM-CSF/IFN-γ-Mediated Inflammation During Spontaneous Spinal Cord Regeneration.Neuroscience bulletin · 2020Article
- Inhibition of lncRNA DILC attenuates neuropathic pain via the SOCS3/JAK2/STAT3 pathway.Bioscience reports · 2020Article
- Upregulation of suppressor of cytokine signaling 3 ameliorates spinal degenerative disease in adolescents by mediating leptin and tumor necrosis factor-α levels.Experimental and therapeutic medicine · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The present study investigates the endogenous expression of Suppressor of Cytokine Signaling-3 (SOCS3) after spinal cord injury (SCI) and its effect on SCI-induced cell death in vivo. In addition, we determined whether a reduction of SOCS3 expression induced by microinjection of short hairpin RNA (shSOCS3) carried by lentivirus into spinal cord provides cellular protection after SCI. We demonstrated that complete transection of rat T8 spinal cord induced SOCS3 expression at the mRNA and protein levels as early as 2days post-injury, which was maintained up to 14days. SOCS3 immunoreactivity was detected in neurons and activated microglia after SCI. We also demonstrated that SCI induces phosphorylation of proteins that are involved in signal transduction and transcription-3 (STAT3) in neurons, which induced SOCS3 expression. Western blot analyses and double-immunofluorescent staining showed significant up-regulation of the pro-apoptotic protein Bax, increases in the ratio of Bax to the anti-apoptotic protein Bcl-2, and up-regulation of cleaved caspase-3 in neurons. Treatment with shSOCS3 inhibited SCI-induced mRNA expression of SOCS3 2days post-injury and suppressed SCI-induced Bax expression 7days after SCI, both rostral and caudal to the lesion. Moreover, treatment with shSOCS3 inhibited SCI-induced neuronal death and protected neuronal morphology both rostral and caudal to the injury site 7days post-injury. Our results suggest that the STAT3/SOCS3 signaling pathway plays an important role in regulating neuronal death after SCI.
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