ArticleNeurobiology of disease2016
STAT3 and SOCS3 regulate NG2 cell proliferation and differentiation after contusive spinal cord injury.
Article in Neurobiology of disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 74 citations in OpenAlex.
- Neuroinflammation in Alzheimer's and Parkinson's diseases: pathogenic mechanisms and therapeutic strategies.Translational neurodegeneration · 2026Review
- Pen-2 regulates glial homeostasis by coordinating self-renewal and transdifferentiation programs in oligodendrocyte precursor cells.Stem cell reports · 2025Article
- Heterogeneous fibroblasts contribute to fibrotic scar formation after spinal cord injury in mice and monkeys.Nature communications · 2024Article
- Article
- Identification and validation of SOCS1/2/3/4 as potential prognostic biomarkers and correlate with immune infiltration in glioblastoma.Journal of cellular and molecular medicine · 2023Article
- Understanding the Role of the Glial Scar through the Depletion of Glial Cells after Spinal Cord Injury.Cells · 2023Review
- Tackling the glial scar in spinal cord regeneration: new discoveries and future directions.Frontiers in cellular neuroscience · 2023Review
- Retinal ganglion cell expression of cytokine enhances occupancy of NG2 cell-derived astrocytes at the nerve injury site: Implication for axon regeneration.Experimental neurology · 2022Article
- Review
- Effects of electroacupuncture on the functionality of NG2-expressing cells in perilesional brain tissue of mice following ischemic stroke.Neural regeneration research · 2022Article
- Circulating microRNA sequencing revealed miRNome patterns in hematology and oncology patients aiding the prognosis of invasive aspergillosis.Scientific reports · 2022Article
- Loss-of-function manipulations to identify roles of diverse glia and stromal cells during CNS scar formation.Cell and tissue research · 2022Review
- The role of neural stem cells in regulating glial scar formation and repair.Cell and tissue research · 2022Review
- Accurate identification of circRNA landscape and complexity reveals their pivotal roles in human oligodendroglia differentiation.Genome biology · 2022Article
- Capacity of astrocytes to promote axon growth in the injured mammalian central nervous system.Frontiers in neuroscience · 2022Review
- Nkx6.1 enhances neural stem cell activation and attenuates glial scar formation and neuroinflammation in the adult injured spinal cord.Experimental neurology · 2021Article
- Single-cell analysis of the cellular heterogeneity and interactions in the injured mouse spinal cord.The Journal of experimental medicine · 2021Article
- Targeted inhibition of STAT3 in neural stem cells promotes neuronal differentiation and functional recovery in rats with spinal cord injury.Experimental and therapeutic medicine · 2021Article
- Myelin Debris Stimulates NG2/CSPG4 Expression in Bone Marrow-Derived Macrophages in the Injured Spinal Cord.Frontiers in cellular neuroscience · 2021Article
- Deciphering glial scar after spinal cord injury.Burns & trauma · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
NG2 cells, also known as oligodendrocyte progenitors or polydendrocytes, are a major component of the glial scar that forms after spinal cord injury. NG2 cells react to injury by proliferating around the lesion site and differentiating into oligodendrocytes and astrocytes, but the molecular mechanism is poorly understood. In this study, we tested the role of the transcription factor STAT3, and its suppressor SOCS3, in NG2 cell proliferation and differentiation after spinal cord injury. Using knockout mice in which STAT3 or SOCS3 are genetically deleted specifically in NG2 cells, we found that deletion of STAT3 led to a reduction in oligodendrogenesis, while deletion of SOCS3 led to enhanced proliferation of NG2 cells within the glial scar after spinal cord injury. Additionally, STAT3 and SOCS3 were not required for astrogliogenesis from NG2 cells after spinal cord injury. Interestingly, genetic deletion of STAT3 and SOCS3 did not have opposing effects, suggesting that SOCS3 may have targets other than the STAT3 pathway in NG2 cells after spinal cord injury. Altogether, our data show that both STAT3 and SOCS3 play important, yet unexpected, roles in NG2 cell proliferation and differentiation after spinal cord injury.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.