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Experimental Demyelination and Remyelination of Murine Spinal Cord by Focal Injection of Lysolecithin
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Modulating proteoglycan receptor PTPσ using intracellular sigma peptide improves remyelination and functional

Parvin Niknam1, Mohammad Reza Raoufy1, Yaghoub Fathollahi1

  • 1Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.

Molecular and Cellular Neurosciences
|July 6, 2019
PubMed

Insights

Intracellular sigma peptide (ISP) inhibits PTPσ signaling, reducing demyelination and astrogliosis in multiple sclerosis models. This promotes myelin repair and restores visual function, offering a new therapeutic strategy for CNS repair.

Area of Science:

  • Neuroscience
  • Immunology
  • Regenerative Medicine

Background:

  • Multiple sclerosis (MS) involves central nervous system (CNS) damage, with glial scars containing chondroitin sulfate proteoglycans (CSPGs) inhibiting repair.
  • CSPGs impede repair by signaling through receptors like protein tyrosine phosphatase sigma (PTPσ).

Purpose of the Study:

  • To investigate the therapeutic potential of intracellular sigma peptide (ISP), a PTPσ inhibitor, in a mouse model of demyelination relevant to MS.
  • To evaluate ISP's effects on myelin repair, glial scarring, and functional recovery in the optic pathway.

Main Methods:

  • Induced focal demyelination in the mouse optic chiasm using lysophosphatidylcholine (LPC).
  • Administered ISP to assess its impact on demyelination, astrogliosis, oligodendrocyte regeneration, and remyelination.
  • Evaluated functional recovery using electrophysiological (visual evoked potential) and behavioral (visual cliff test) assessments.

Main Results:

  • ISP treatment significantly decreased demyelination and astrogliosis.
  • ISP administration increased the generation of new oligodendrocytes, leading to enhanced remyelination.
  • Electrophysiological and behavioral tests demonstrated improved optic pathway integrity and visual acuity with ISP treatment.
  • ISP showed regenerative effects even when administered solely during the repair phase.

Conclusions:

  • ISP effectively inhibits PTPσ signaling, promoting myelin protection and repair in demyelinated axons.
  • ISP demonstrates potential as a novel therapeutic strategy for restoring neural pathway conductivity and visual function in MS patients.
  • Targeting PTPσ with ISP offers a promising approach for CNS repair in demyelinating diseases.
Keywords:
Chondroitin sulfate proteoglycans (CSPG)MouseMultiple sclerosisMyelin repairOligodendrocyte, intracellular sigma peptide (ISP)Protein tyrosine phosphatase sigma (PTPσ)

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