NT-3 Promotes Oligodendrocyte Proliferation and Nerve Function Recovery After Spinal Cord Injury by Inhibiting Autophagy Pathway
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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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].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [452]
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Autophagy and ALS: mechanistic insights and therapeutic implications
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“Paradoxically, suppression of autophagy with NTF3 (neurotrophin 3) disinhibits oligodendrocyte proliferation and promotes motor recovery in a separate model of spinal cord contusion [452].”
Background
- 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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