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Cited by 2Nerve injury and regenerationSpinal Cord Injury ResearchPain Mechanisms and Treatments

Ptbp1 Knockdown in Glial Cells Promotes Motor and Sensory Function Recovery After Peripheral Nerve Injury

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Song, Honghao, Peng, Lei, Chen, Dashuang, Fan, Xiaoyi, Hua, Tong, Ding, Ruifeng, Deng, Mengqiu, Chen, Qianbo +2 more·2025·CNS Neuroscience & Therapeutics
DOI 10.1111/cns.70531PMC PMC12287381
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Abstract

Background: Peripheral nerve injury (PNI) frequently causes persistent sensory and motor deficits with limited therapeutic options. While Ptbp1‐mediated astrocyte reprogramming shows promise in central nervous system repair, its role in PNI—particularly regarding spinal cord astrocytes and dorsal root ganglia (DRG) satellite glial cells (SGCs)—remains unexplored.Aims: This study aimed to determine whether Ptbp1 knockdown in glial cells enhances functional recovery after sciatic nerve injury (SNI) by dual mechanisms: (1) converting spinal cord astrocytes to motor neurons and polarizing them toward neuroprotective A2 phenotype, and (2) activating regenerative signaling pathways in DRG SGCs.Materials & Methods: C57BL/6J mice underwent SNI followed by intrathecal injection of AAV‐GFAP‐CasRx‐Ptbp1 (targeting Ptbp1 in astrocytes/SGCs) or control virus. Primary astrocytes and SGCs were transfected with Ptbp1 siRNA in vitro. Assessments included functional recovery (Basso Mouse Scale, Louisville Swim Score, Hargreaves test, von Frey assay), axonal regeneration (HE/β3‐tubulin/SCG‐10 staining), transcriptome/ATAC sequencing, and molecular analyses (immunofluorescence for DCX/Islet1/ntng2‐NGL‐2; Western blot for Ptbp1/GDNF/C3).Results: Ptbp1 was upregulated in spinal cord astrocytes and DRG SGCs post‐SNI. Its knockdown accelerated motor/sensory functional recovery and axonal regeneration. Mechanistically, in the spinal cord, Ptbp1 depletion induced astrocyte‐to‐motor neuron conversion (upregulation of DCX/Islet1/Map2) and polarized astrocytes toward A2 phenotype (upregulation of S100a10/GDNF; downregulation of C3). In DRG, it activated the ntng2/NGL‐2 pathway in SGCs, enhancing sensory axon regeneration (upregulation of ATF3/GAP43). Ntng2 blockade abolished sensory regeneration, confirming pathway dependence.Discussion: Ptbp1 knockdown promotes PNI repair through spatially distinct mechanisms: spinal cord astrocyte reprogramming/A2 polarization synergizes with DRG SGC‐mediated ntng2/NGL‐2 activation. While astrocyte‐to‐neuron conversion was limited, dominant A2 polarization provided neuroprotection. The absence of SGC transdifferentiation highlights cell‐type‐specific responses. Limitations include low conversion efficiency and interspecies regenerative differences.Conclusion: Targeting Ptbp1 in glial cells accelerates PNI recovery by dual regenerative mechanisms: motor function restoration via astrocyte‐derived neuron replenishment and A2 polarization, coupled with sensory repair through ntng2/NGL‐2 pathway activation. This establishes Ptbp1 as a promising therapeutic target for nerve injuries.

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  • Early studies reported that suppressing PTBP1 in astrocytes or other glia could initiate neuronal transcriptional programs and produce cells resembling functional neurons in models of Parkinson's disease and retinal injury.

    “Early studies reported that suppressing PTBP1 in astrocytes or other glia could initiate neuronal transcriptional programs and produce cells resembling functional neurons in models of Parkinson’s disease and retinal injury, sparking strong enthusiasm for PTBP1 as a single-factor reprogramming node.”

    From Reverse the progression of Alzheimer’s disease through Nano-ERASER-based adult neuroregeneration (2026) · cites this paper as [13]

    The Discussion (page unavailable) reports that an earlier Parkinson’s disease mouse study converted midbrain astrocytes into dopaminergic neurons after Ptbp1 knockdown. The Introduction describes substantial interest in the approach, but the copy does not report production of neuron-like cells in a retinal-injury model; its discussion of optic nerve injury concerns protective effects, and its cited retinal study reports no glia-to-neuron conversion. (LLM, conf=0.85)

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Cited by

Sorted by citations

Authors
Song, H., Peng, L., Chen, D., Fan, X., Hua, T., Ding, R., Deng, M., Chen, Q., Yang, M., & Yuan, H.
Affiliations
  • Second Military Medical University (CN)
  • Department of Anesthesiology Changzheng Hospital, Naval Medical University Shanghai People's Republic of China
Corresponding author
  • Chen, Qianbo
  • Yang, Mei
  • Yuan, Hongbin
ORCID
Venue
CNS Neuroscience & Therapeutics
Publisher
Wiley
Published
2025-07
Volume
31
Issue
7
Pages
e70531-e70531
ISSN
  • 1755-5930 (ISSN-L)
  • 1755-5949
DOI
10.1111/cns.70531
PMC
PMC12287381
OpenAlex
W4412645668
Cited by
2
References
2
Citations by year
2026: 2
FWCI
0.78
Type
journal article
Language
en
Open access
Licence
Locations
  • CNS Neuroscience & Therapeutics (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
Keywords
PTBP1, peripheral nerve injury, sciatic nerve injury, glial cells, spinal astrocytes, satellite glial cells, dorsal root ganglia, sensory axon regeneration, motor recovery, sensory recovery, axon regeneration, glial cell line-derived neurotrophic factor
MeSH terms
Doublecortin Protein, Animals, Astrocytes, Cells, Cultured, Ganglia, Spinal, Male, Mice, Inbred C57BL, Motor Neurons, Nerve Regeneration, Neuroglia, Recovery of Function, Heterogeneous-Nuclear Ribonucleoproteins, Polypyrimidine Tract-Binding Protein, Mice, Gene Knockdown Techniques, Peripheral Nerve Injuries

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