Apamin administration impact on miR-219 and miR-155-3p expression in cuprizone induced multiple sclerosis model

Samira Gholami1, Mina Mirian2, Seyed Mehdi Eftekhari3

  • 1School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences and Health Services, Isfahan, Iran.

Molecular Biology Reports
|November 11, 2020
PubMed

Insights

Apamin peptide may reduce multiple sclerosis (MS) plaque formation by modulating miR-155-3p during demyelination. This offers a potential therapeutic strategy for MS exacerbations.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Multiple sclerosis (MS) is a chronic central nervous system disease impacting myelination.
  • MicroRNAs (miRNAs) like miR-219 and miR-155-3p are implicated in MS pathogenesis.
  • Apamin, a peptide toxin, is being investigated for its therapeutic potential in MS.

Purpose of the Study:

  • To investigate the role of miR-219 and miR-155-3p in the myelination process of an MS model.
  • To evaluate the effect of apamin peptide administration on miRNA expression and myelination in MS.

Main Methods:

  • A cuprizone-induced mouse model of multiple sclerosis was utilized.
  • Apamin peptide was administered during demyelination (phase I) or remyelination (phase II) phases.
  • Myelin content was assessed using Luxol Fast Blue (LFB) staining, and microRNA levels were quantified via Real-Time PCR.

Main Results:

  • miR-219 was downregulated in phase I (demyelination) compared to controls.
  • Apamin co-treatment significantly inhibited miR-155-3p upregulation during phase I.
  • Apamin demonstrated a greater effect on reducing miR-155-3p in phase I than on miR-219 in phase II.

Conclusions:

  • Dysregulation of miR-219 and miR-155-3p occurs during different phases of MS.
  • Apamin peptide shows therapeutic potential in mitigating MS plaque formation, particularly during the exacerbation phase.
  • Modulation of miR-155-3p by apamin suggests a novel therapeutic avenue for MS treatment.

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