Cited by 32Spinal Cord Injury ResearchNerve injury and regenerationNeurogenesis and neuroplasticity mechanisms

NT-3 Promotes Oligodendrocyte Proliferation and Nerve Function Recovery After Spinal Cord Injury by Inhibiting Autophagy Pathway

Cong, Yan, Wang, Chunqing, Wang, Jiyao, Li, Hexiang, Li, Qing·2020·Journal of Surgical Research

Abstract

Background Spinal cord injury (SCI) is a serious medical problem, leading to lifelong disability and increasing the health burden worldwide. Traditional treatments have limited effects on neuronal function recovery. Previous studies showed that neurotrophin-3 (NT-3) promoted oligodendrocyte survival and improved neuronal functional recovery after SCI. However, the mechanism by which NT-3 promotes oligodendrocyte survival after SCI remains unclear, which limits its application.Materials and methods A total of 75 female Sprague-Dawley rats were randomly divided into three groups: the NS group, NT-3 group, and NT-3 + rapamycin group. After successful modeling, the spinal cord specimens were taken at the corresponding time points. Western blot was used to detect autophagy-related proteins and Olig1 protein expression and combined with pathology, immunohistochemistry, flow cytometry, and other methods to detect the proliferation of oligodendrocytes after NT-3 application.Results NT-3 was found to significantly promote the recovery of motor function by Basso-Beattie-Bresnahan scores analysis in the rat SCI model. Furthermore, intraspinal administration of NT-3 could downregulate the expression of Beclin-1 in oligodendrocytes, indicating that NT-3 could inhibit excessive autophagy of oligodendrocytes after SCI. The effects of NT-3 on oligodendrocyte survival could be blocked by an autophagy activator rapamycin.Conclusions This study found that NT-3 could promote the recovery of motor function after SCI in rats. The underlying reason may be that NT-3 inhibits the expression of autophagy proteins in oligodendrocytes and promotes oligodendrocyte proliferation. This study provided evidence for the future clinical application of NT-3 in SCI patients.

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Crossref · 10.1016/j.jss.2019.10.033

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  • Suppression of autophagy with NTF3 disinhibits oligodendrocyte proliferation and promotes motor recovery in a separate model of spinal cord contusion.

    “Paradoxically, suppression of autophagy with NTF3 (neurotrophin 3) disinhibits oligodendrocyte proliferation and promotes motor recovery in a separate model of spinal cord contusion [452].”

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Authors
Cong, Y., Wang, C., Wang, J., Li, H., & Li, Q.
Affiliations
  • Guiyang Medical University (CN)
  • Affiliated Hospital of Guizhou Medical University (CN)
Corresponding author
Wang, Chunqing
Venue
Journal of Surgical Research
Publisher
Elsevier BV
Published
2020-03
Volume
247
Pages
128-135
ISSN
0022-4804 (ISSN-L)
OpenAlex
W2989561666
Cited by
32
References
35
Citations by year
2026: 3 · 2025: 3 · 2024: 6 · 2023: 6 · 2022: 6 · 2021: 5 · 2020: 3
FWCI
2.58
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Surgical Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords
neurotrophin-3, spinal cord injury, oligodendrocyte proliferation, autophagy inhibition, Beclin-1, motor recovery, rapamycin, Olig1, oligodendrocyte survival, neurotrophic therapy
MeSH terms
Beclin-1, Animals, Autophagy, Cell Survival, Disease Models, Animal, Female, Humans, Motor Activity, Nerve Tissue Proteins, Oligodendroglia, Spinal Cord Injuries, Spinal Nerves, Signal Transduction, Rats, Sprague-Dawley, Sirolimus, Recovery of Function, Neurotrophin 3, Cell Proliferation, Rats, Basic Helix-Loop-Helix Proteins, Basic Helix-Loop-Helix Transcription Factors

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