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Exosomes from mesenchymal stem cells expressing miR-125b inhibit neointimal hyperplasia via myosin IE

Dongqing Wang1,2, Bin Gao3, Jianing Yue1

  • 1Department of Vascular Surgery, Zhongshan Hospital Fudan University, Shanghai, China.

Journal of Cellular and Molecular Medicine
|November 29, 2018
PubMed

Insights

Mesenchymal stem cell-derived exosomes (MSC-Exo) inhibit vascular smooth muscle cell proliferation and neointimal hyperplasia. MSC-Exo transfer miR-125b, which represses Myo1e, offering a potential therapeutic strategy for vascular diseases.

Area of Science:

  • Regenerative Medicine
  • Vascular Biology
  • Cellular and Molecular Biology

Background:

  • Mesenchymal stem cells (MSCs) communicate with target cells via exosomes, influencing the perivascular environment.
  • The role of exosome-mediated microRNA transfer in neointimal hyperplasia is not well understood.

Purpose of the Study:

  • To investigate the effects of MSC-derived exosomes (MSC-Exo) on neointimal hyperplasia.
  • To elucidate the underlying molecular mechanisms, including microRNA transfer and target gene regulation.

Main Methods:

  • Assessed MSC-Exo effects on vascular smooth muscle cell (VSMC) proliferation and migration in vitro.
  • Utilized a balloon-induced vascular injury model in vivo to evaluate neointimal hyperplasia.
  • Identified and quantified microRNAs within MSC-Exo, focusing on miR-125b and its target gene, myosin 1E (Myo1e).

Main Results:

  • MSC-Exo were internalized by VSMCs, inhibiting their proliferation and migration in vitro.
  • miR-125b was found to be enriched in MSC-Exo and targeted the 3' untranslated region of Myo1e, repressing its expression.
  • MSC-Exo and transferred miR-125b suppressed Myo1e expression, VSMC proliferation, migration, and neointimal hyperplasia in vivo.

Conclusions:

  • MSC-Exo inhibit VSMC proliferation and neointimal hyperplasia by transferring miR-125b.
  • The miR-125b/Myo1e axis plays a critical role in regulating neointimal hyperplasia.
  • MSC-Exo and miR-125b represent potential therapeutic targets for vascular diseases.
Keywords:
Myo1eexosomemesenchymal stem cellsmiR-125bneointimal hyperplasia

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