ArticleCardiovascular research2020
Endothelial microvesicles carrying Src-rich cargo impair adherens junction integrity and cytoskeleton homeostasis.
Article in Cardiovascular research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 57 citations in OpenAlex.
- Extracellular Vesicles as Drivers of Lung Endothelial Dysfunction in ARDS: Mechanisms and Therapeutic Opportunities.Comprehensive Physiology · 2026Review
- Microbial landscapes in dairy cow diseases: from localized dysbiosis to inter-organ axes.NPJ biofilms and microbiomes · 2026Review
- Barrier breakdown: lung-brain crosstalk in systemic inflammation.Journal of neuroinflammation · 2026Review
- Mechanisms of Yiqi Huoxue Granule in Atherosclerosis Treatment: Insights from UPLC-Q-Exactive Orbitrap-MS Analysis, Network Pharmacology, Molecular Docking, and Experimental Verification.Journal of inflammation research · 2026Article
- Neutrophil-secreted extracellular vesicles induce blood-brain barrier leakage and tight junction disruption.Fluids and barriers of the CNS · 2025Article
- Two Sides of the Same Coin-Mechanistic Insight, Diagnostic Application and Therapeutic Translation of Bacterial and Host-Derived Extracellular Vesicles.Journal of extracellular biology · 2025Review
- Farrerol ameliorates diabetic cardiomyopathy by inhibiting ferroptosisWorld journal of diabetes · 2025Article
- Lung endothelial cell senescence impairs barrier function and promotes neutrophil adhesion and migration.GeroScience · 2025Article
- Stem cell-derived exosome delivery systems for treating atherosclerosis: The new frontier of stem cell therapy.Materials today. Bio · 2025Review
- An approach to evaluate the effect of inflammatory microvesicles on CaExperimental biology and medicine (Maywood, N.J.) · 2025Article
- Pathogenic and therapeutic roles of extracellular vesicles in sepsis.Frontiers in immunology · 2025Review
- Neutrophil extracellular traps: a catalyst for atherosclerosis.Molecular and cellular biochemistry · 2024Review
- Extracellular Vesicles as Mediators in Atherosclerotic Cardiovascular Disease.Journal of lipid and atherosclerosis · 2024Review
- Review
- S1PR3 inhibition protects against LPS-induced ARDS by inhibiting NF-κB and improving mitochondrial oxidative phosphorylation.Journal of translational medicine · 2024Article
- Microvesicles derived from dermal myofibroblasts modify the integrity of the blood and lymphatic barriers using distinct endocytosis pathways.Journal of extracellular biology · 2024Article
- Global trends in research on endothelial cells and sepsis between 2002 and 2022: A systematic bibliometric analysis.Heliyon · 2024Review
- Exosome-Derived microRNA: Potential Target for Diagnosis and Treatment of Sepsis.Journal of immunology research · 2024Review
- Entry and exit of extracellular vesicles to and from the blood circulation.Nature nanotechnology · 2024Review
- Extracellular Vesicles in Atherosclerosis: State of the Art.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
aimsMicrovesicles (MVs) conduct intercellular communication and impact diverse biological processes by transferring bioactive cargos to other cells. We investigated whether and how endothelial production of MVs contribute to vascular dysfunction during inflammation. METHODS AND
resultsWe measured the levels and molecular properties of endothelial-derived MVs (EC-MVs) from mouse plasma following a septic injury elicited by cecal ligation and puncture, as well as those from supernatants of cultured endothelial cells stimulated by inflammatory agents including cytokines, thrombin, and complement 5a. The mouse studies showed that sepsis caused a significant increase in total plasma vesicles and VE-cadherin+ EC-MVs compared to sham control. In cultured ECs, different inflammatory agents caused diverse patterns of EC-MV production and cargo contents. When topically applied to endothelial cells, EC-MVs induced a cytoskeleton-junction response characterized by myosin light chain phosphorylation, contractile fibre reorganization, VE-cadherin phosphorylation, and adherens junction dissociation, functionally measured as increased albumin transendothelial flux and decreased barrier resistance. The endothelial response was coupled with protein tyrosine phosphorylation promoted by MV cargo containing c-Src kinase, whereas MVs produced from c-Src deficient cells did not exert barrier-disrupting effects. Additionally, EC-MVs contribute to endothelial inflammatory injury by promoting neutrophil-endothelium adhesion and release of neutrophil extracellular traps containing citrullinated histones and myeloperoxidase, a response unaltered by c-Src knockdown.
conclusionEndothelial-derived microparticles cause endothelial barrier dysfunction by impairing adherens junctions and activating neutrophils. The signalling mechanisms underlying the endothelial cytoskeleton-junction response to EC-MVs involve protein phosphorylation promoted by MV cargo carrying c-Src. However, EC-MV-induced neutrophil activation was not dependent on c-Src.
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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.