Related Experiment Video

Updated: Jun 23, 2025

Synergetic Use of Neural Precursor Cells and Self-assembling Peptides in Experimental Cervical Spinal Cord Injury
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Synergetic Use of Neural Precursor Cells and Self-assembling Peptides in Experimental Cervical Spinal Cord Injury

Published on: February 23, 2015

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Inhibition of CSPG-PTPσ Activates Autophagy Flux and Lysosome Fusion, Aids Axon and Synaptic Reorganization in Spinal

Hongyu Wang1,2,3,4, Naibo Feng5,6, Chungeng Liu5,6

  • 1The First Affiliated Hospital (Shenzhen People's Hospital), Southern University of Science and Technology, Shenzhen, 518055, China. wanghongyu790039663@126.com.

Molecular Neurobiology
|June 20, 2024
PubMed

Insights

Intracellular sigma peptide (ISP) activates autophagy and promotes synaptic reorganization after spinal cord injury (SCI). This treatment improves motor neuron survival and functional recovery, highlighting a new therapeutic avenue for SCI.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Regenerative Medicine

Background:

  • Chondroitin sulfate proteoglycans (CSPGs) and their receptor protein tyrosine phosphatase σ (PTPσ) are implicated in spinal cord injury (SCI) pathology.
  • Autophagy inhibition can induce CSPGs in astrocytes, but CSPG's influence on autophagy and its role in SCI remain unclear.

Purpose of the Study:

  • To investigate the effects of intracellular sigma peptide (ISP), which targets PTPσ, on autophagy and synaptic reorganization in the context of SCI.
  • To elucidate the therapeutic potential of ISP in promoting recovery after spinal cord injury.

Main Methods:

  • Utilized western blotting to assess autophagy markers (LC3B-II/I, p62) and autophagosome-lysosome fusion proteins (STX17, LAMP2).
  • Quantified pre- and post-synaptic markers (SYN, PSD-95, VGLUT1), axon markers (neurofilament, GAP-43), and motor neuron survival.
  • Evaluated neurobehavioral recovery in an SCI model.

Main Results:

  • ISP treatment activated autophagy flux by increasing LC3B-II/I and decreasing p62.
  • ISP restored autophagosome-lysosome fusion, evidenced by increased STX17 and LAMP2 levels.
  • ISP enhanced synaptic reorganization, promoted axon growth, preserved motor neurons, and improved neurobehavioral outcomes in SCI models.

Conclusions:

  • ISP targeting PTPσ activates autophagy flux, facilitates synaptic reorganization, and promotes functional recovery after SCI.
  • ISP demonstrates therapeutic potential for mitigating SCI pathology and enhancing recovery by influencing CSPG-PTPσ signaling and autophagy.
Keywords:
Autophagy fluxCSPGLysosome fusionPTPσSpinal cord injury

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