ArticleCell death & disease2019
Exosomes derived from M1 macrophages aggravate neointimal hyperplasia following carotid artery injuries in mice through miR-222/CDKN1B/CDKN1C pathway.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed.
- M1 macrophage-derived exosomal miR-155-5p exacerbates aortic dissection via SMAD5-Mediated regulation of vascular smooth muscle cell phenotype.Bioactive materials · 2026Article
- The role of non-coding RNAs derived from macrophage exosomes in cardiovascular diseases.The Journal of physiology · 2026Review
- Membrane Vesicles ImproveMicroorganisms · 2026Article
- Research progress on the effects of macrophage‑derived exosomes on muscle factors IGF‑1 and FGF‑2 mediating musculoskeletal crosstalk molecular signaling pathway on bone metabolism (Review).International journal of molecular medicine · 2026Review
- Global Research Landscape in T Cells and Myasthenia Gravis: Trends, Collaborations, and Future Directions.Molecular neurobiology · 2026Review
- Development of a Novel Murine Model of In-Stent Neoatherosclerosis.Journal of the American Heart Association · 2025Article
- Myeloid-specific deficiency of ribosomal protein L13a alters macrophage polarity and diversity during differentiation from bone marrow.Journal of leukocyte biology · 2025Article
- Role of Exosomes in Cardiovascular Disease: A Key Regulator of Intercellular Communication in Cardiomyocytes.ACS omega · 2025Review
- Exosome-mediated effects of BRCA1 on cardiovascular artery disease.Cell biology and toxicology · 2025Article
- Harnessing extracellular vesicles to tame inflammation: a new strategy for atherosclerosis therapy.Frontiers in immunology · 2025Review
- Macrophage-driven exosomes regulate the progression of cardiovascular disease.Frontiers in pharmacology · 2025Review
- The Nf1-Q181X point mutation induces M2 macrophage polarization via the AKT/STAT pathway to promote smooth muscle cell proliferation and migration.Molecular biology reports · 2024Article
- Exploring the Role of Extracellular Vesicles in Skeletal Muscle Regeneration.International journal of molecular sciences · 2024Review
- The effect of macrophages and their exosomes in ischemic heart disease.Frontiers in immunology · 2024Review
- Effect of radiotherapy on the DNA cargo and cellular uptake mechanisms of extracellular vesicles.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023Review
- Circulating small extracellular vesicles promote proliferation and migration of vascular smooth muscle cells via AXL and MerTK activation.Acta pharmacologica Sinica · 2023Article
- Emerging role of exosomes in vascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Role of Circulating Exosomes in Cerebrovascular Diseases: A Comprehensive Review.Current neuropharmacology · 2023Review
- Article
- Diabetic macrophage small extracellular vesicles-associated miR-503/IGF1R axis regulates endothelial cell function and affects wound healing.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of M1 macrophages (M1M)-derived exosomes in the progression of neointimal hyperplasia remains unclear now. Using a transwell co-culture system, we demonstrated that M1M contributed to functional change of vascular smooth muscle cell (VSMC). We further stimulated VSMCs with exosomes isolated from M1M. Our results demonstrated that these exosomes could be taken up by VSMCs through macropinocytosis. Using a microRNA array assay, we identified that miR-222 originated from M1M-derived exosomes triggered the functional changes of VSMCs. In addition, we confirmed that miR-222 played a key role in promoting VSMCs proliferation and migration by targeting Cyclin Dependent Kinase Inhibitor 1B (CDKN1B) and Cyclin Dependent Kinase Inhibitor 1C (CDKN1C) in vitro. In vivo, M1M-derived exosomes significantly aggravated neointima formation following carotid artery ligation injury and wire injury and these effects were partly abolished by miR-222 inhibitor 2'OMe-miR-222. Our findings thus suggest that exosomes derived from M1M could aggravate neointimal hyperplasia through delivering miR-222 into VSMCs. Future studies are warranted to validate if the post-injury vascular neointimal hyperplasia and restenosis could be attenuated by inhibiting miR-222.
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