Bone marrow-derived mesenchymal stem cells microvesicles stabilize atherosclerotic plaques by inhibiting

Yu Lin1, Meihan Liu2, Enqi Chen2

  • 1Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.

Cell Biology International
|December 16, 2020
PubMed

Insights

Bone marrow-derived mesenchymal stem cells microvesicles (BMSCs-MVs) stabilize atherosclerotic plaques by reducing inflammation and pyroptosis. These microvesicles carry microRNA-223 (miR-223) to inhibit NLRP3 expression, offering a novel therapeutic strategy for atherosclerosis.

Area of Science:

  • Cardiovascular Research
  • Stem Cell Biology
  • Molecular Medicine

Background:

  • Atherosclerotic plaque rupture is a primary cause of thrombosis and acute ischemic coronary syndrome.
  • Bone marrow-derived mesenchymal stem cells microvesicles (BMSCs-MVs) show potential in promoting angiogenesis.
  • The role of BMSCs-MVs in stabilizing atherosclerotic plaques requires further investigation.

Purpose of the Study:

  • To investigate the therapeutic potential of BMSCs-MVs in stabilizing atherosclerotic plaques.
  • To elucidate the underlying molecular mechanisms, including the involvement of microRNA-223 (miR-223) and NLRP3 inflammasome.

Main Methods:

  • Isolation and characterization of BMSCs-MVs in a mouse model of atherosclerosis.
  • In vitro studies using a macrophage model with high glucose and oxidative damage.
  • Detection of NLRP3, pyroptosis-related proteins, inflammatory factors, and miR-223.
  • Experimental manipulation of miR-223 and NLRP3 expression.

Main Results:

  • BMSCs-MVs reduced atherosclerotic plaque vulnerability and intima-media thickness in mice.
  • BMSCs-MVs inhibited pyroptosis and inflammatory factor release in macrophages.
  • BMSCs-MVs delivered miR-223, which directly targeted and inhibited NLRP3 expression, thereby reducing pyroptosis.

Conclusions:

  • BMSCs-MVs demonstrate significant plaque-stabilizing effects in atherosclerosis.
  • The therapeutic action of BMSCs-MVs is mediated by the miR-223/NLRP3 pathway, suppressing macrophage pyroptosis and inflammation.
  • BMSCs-MVs represent a promising cell-free therapy for atherosclerosis management.