ArticleCardiovascular research2023
Rapid neutrophil mobilization by VCAM-1+ endothelial cell-derived extracellular vesicles.
Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
47 citing papers in PubMed, 55 citations in OpenAlex.
- Pharmacological Inhibition of Small Extracellular Vesicle Secretion by ALK5i SD-208 via Lysosomal Rerouting of CD63+ Compartments.Journal of extracellular vesicles · 2026Article
- Extracellular Vesicles in Cardiac Cell Crosstalk: from Intercellular Communication to Clinical Translation.Cardiovascular drugs and therapy · 2026Review
- Polarized release of brain microvascular endothelial cell- derived extracellular vesicles is functionally coupled to leukocyte transendothelial migration.Research square · 2026Article
- The spleen-heart crosstalk in cardiovascular disease: integrating neural, immune, and secretory pathways.Acta pharmacologica Sinica · 2026Review
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- Dynamics of neutrophilia at the neurovascular unit arising from repeated pulmonary inflammation.Journal of neuroinflammation · 2026Article
- Plasma extracellular vesicle modulate immune cell transcriptional responses following acute myocardial infarction.iScience · 2026Article
- Alterations in endothelial activation biomarkers ICAM-1 and VCAM-1 following mitral regurgitation surgery.Turkish journal of surgery · 2026Article
- HDL Regulates TGFβ-Receptor Lipid Raft Partitioning, Restoring Contractile Features of Cholesterol-Loaded Vascular Smooth Muscle Cells.JACC. Basic to translational science · 2026Article
- Neutrophils and neutrophil extracellular traps in ischaemia-reperfusion injury: pathophysiological roles and therapeutic potential.Burns & trauma · 2026Review
- miRNAs-neutrophil axis: novel insights into acute lung injury and chronic inflammatory lung diseases.Frontiers in immunology · 2026Review
- The role of microRNAs in cardiovascular disease associated with the consumption of ultra-processed foods: a comprehensive review.Frontiers in nutrition · 2026Review
- Spatial immune niche remodeling of the neutrophil-macrophage axis inchronic liver disease.Frontiers in cell and developmental biology · 2026Review
- Acute Myocardial Infarction: Molecular Pathogenesis, Diagnosis, and Clinical Management.MedComm · 2025Review
- The spleen in ischaemic heart disease.Nature reviews. Cardiology · 2025Review
- Mir-509-3p targets SLC25A13 to regulate ferroptosis and protect retinal endothelial cells in diabetic retinopathy.Acta diabetologica · 2025Article
- Endothelial HSPA12B regulates myocardial monocyte infiltration and inflammatory activity after myocardial infarction.Frontiers in immunology · 2025Article
- Indoleamine 2,3-dioxygenase-galectin-3 fusion protein remodels inflammatory and fibrotic programs, ameliorating imiquimod-induced psoriasis.npj biomedical innovations · 2025Article
- Article
- Emerging opportunities to target inflammation: myocardial infarction and type 2 diabetes.Cardiovascular research · 2024Review
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34 authors at 9 institutions in 5 countries.
Funding
Abstract
aimsAcute myocardial infarction rapidly increases blood neutrophils (<2 h). Release from bone marrow, in response to chemokine elevation, has been considered their source, but chemokine levels peak up to 24 h after injury, and after neutrophil elevation. This suggests that additional non-chemokine-dependent processes may be involved. Endothelial cell (EC) activation promotes the rapid (<30 min) release of extracellular vesicles (EVs), which have emerged as an important means of cell-cell signalling and are thus a potential mechanism for communicating with remote tissues. METHODS AND
resultsHere, we show that injury to the myocardium rapidly mobilizes neutrophils from the spleen to peripheral blood and induces their transcriptional activation prior to arrival at the injured tissue. Time course analysis of plasma-EV composition revealed a rapid and selective increase in EVs bearing VCAM-1. These EVs, which were also enriched for miRNA-126, accumulated preferentially in the spleen where they induced local inflammatory gene and chemokine protein expression, and mobilized splenic-neutrophils to peripheral blood. Using CRISPR/Cas9 genome editing, we generated VCAM-1-deficient EC-EVs and showed that its deletion removed the ability of EC-EVs to provoke the mobilization of neutrophils. Furthermore, inhibition of miRNA-126 in vivo reduced myocardial infarction size in a mouse model.
conclusionsOur findings show a novel EV-dependent mechanism for the rapid mobilization of neutrophils to peripheral blood from a splenic reserve and establish a proof of concept for functional manipulation of EV-communications through genetic alteration of parent cells.
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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.