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Updated: Nov 25, 2025

Mesenchymal Stem Cell Regulation of Macrophage Phagocytosis; Quantitation and Imaging
Published on: July 16, 2021
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.
Abstract:
Rupture of atherosclerotic plaques constitutes the major cause of thrombosis and acute ischemic coronary syndrome. Bone marrow-derived mesenchymal stem cells microvesicles (BMSCs-MVs) are reported to promote angiogenesis. This study investigated the role of BMSCs-MVs in stabilizing atherosclerotic plaques. BMSCs-MVs in mice were isolated and identified. The mouse model of atherosclerosis was established, and mice were injected with BMSCs-MVs via the tail vein. The macrophage model with high glucose and oxidative damage was established and then incubated with BMSCs-MVs. Nod-like receptor protein 3 (NLRP3) expression, pyroptosis-related proteins, and inflammatory factors were detected. Actinomycin D was used to inhibit the secretion of BMSCs-MVs to verify the source of microRNA-223 (miR-223). The binding relationship between miR-223 and NLRP3 was predicted and verified. BMSCs-MVs with knockdown of miR-223 were cocultured with bone marrow-derived macrophages with knockdown of NLRP3, and then levels of miR-223, NLRP3, pyroptosis-related proteins, and inflammatory factors were detected. BMSCs-MVs could reduce the vulnerability index of atherosclerotic plaques and intima-media thickness in mice, and inhibit pyroptosis and inflammation. BMSCs-MVs inhibited pyroptosis and inflammatory factors in macrophages. BMSCs-MVs carried miR-223 to inhibit NLRP3 expression and reduce macrophage pyroptosis, thereby stabilizing the atherosclerotic plaques.
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.
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