ArticleThe Journal of international medical research2019
Regulation of capillary tubules and lipid formation in vascular endothelial cells and macrophages via extracellular vesicle-mediated microRNA-4306 transfer.
Article in The Journal of international medical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- Extracellular Vesicle-Associated miR-ERIA Exerts the Antiangiogenic Effect of Macrophages in Diabetic Wound Healing.Diabetes · 2025Article
- The Crosstalk Between Endothelial Cells, Smooth Muscle Cells, and Macrophages in Atherosclerosis.International journal of molecular sciences · 2025Review
- Extracellular vesicles in atherosclerosis cardiovascular disease: emerging roles and mechanisms.Frontiers in cardiovascular medicine · 2025Review
- Endothelial extracellular vesicles: their possible function and clinical significance in diabetic vascular complications.Journal of translational medicine · 2024Review
- Extracellular vesicles in atherosclerosis and vascular calcification: the versatile non-coding RNAs from endothelial cells and vascular smooth muscle cells.Frontiers in medicine · 2023Review
- Lipid metabolism patterns and relevant clinical and molecular features of coronary artery disease patients: an integrated bioinformatic analysis.Lipids in health and disease · 2022Article
- Article
- Recent advances of natural and bioengineered extracellular vesicles and their application in vascular regeneration.Regenerative biomaterials · 2022Review
- Integrative biology of extracellular vesicles in diabetes mellitus and diabetic complications.Theranostics · 2022Review
- Exosomes in atherosclerosis: Convergence on macrophages.International journal of biological sciences · 2022Review
- Identification of Core Genes and Screening of Potential Targets in Intervertebral Disc Degeneration Using Integrated Bioinformatics Analysis.Frontiers in genetics · 2022Article
- Inhibition of LOXL1-AS1 alleviates oxidative low-density lipoprotein induced angiogenesis via downregulation of miR-590-5p mediated KLF6/VEGF signaling pathway.Cell cycle (Georgetown, Tex.) · 2021Article
- Recent advances in Extracellular Vesicles and their involvements in vasculitis.Free radical biology & medicine · 2021Review
- Extracellular Vesicle miRNAs in the Promotion of Cardiac Neovascularisation.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study aimed to examine regulation of capillary tubules and lipid formation in vascular endothelial cells and macrophages via extracellular vesicle-mediated microRNA (miRNA)-4306 transfer.
methodsWhole blood samples (12 mL) were collected from 53 patients, and miR-4306 levels in extracellular vesicles (EVs) were analyzed by reverse transcription-polymerase chain reaction. Human coronary artery vascular endothelial cells (HCAECs) and human monocyte-derived macrophages (HMDMs) were transfected with a scrambled oligonucleotide, an miR-4306 mimic, or an anti-miR-4306 inhibitor. The direct effect of miR-4306 on the target gene was analyzed by a dual-luciferase reporter assay.
resultsEV-contained miR-4306 released from HMDMs was significantly upregulated in coronary artery disease. Oxidized low-density lipoprotein (ox-LDL)-stimulated HMDM-derived EVs inhibited proliferation, migration, and angiogenesis abilities of HCAECs in vitro. However, ox-LDL-stimulated HCAEC-derived EVs enhanced lipid formation of HMDMs. The possible mechanism of these findings was partly due to EV-mediated miR-4306 upregulation of the Akt/nuclear factor kappa B signaling pathway.
conclusionsParacrine cellular crosstalk between HCAECs and HMDMs probably supports the pro-atherosclerotic effects of EVs under ox-LDL stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.