ArticlePloS one2016
Microparticle-Induced Activation of the Vascular Endothelium Requires Caveolin-1/Caveolae.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Novel extracellular vesicle release pathway facilitated by toxic superoxide dismutase 1 oligomers.Neurobiology of disease · 2026Article
- Endothelial microparticles in high glucose environment: molecular pathways of GDM-associated placental dysfunction and coenzyme Q10-based targeted therapy.Journal of nanobiotechnology · 2026Article
- Uremic Toxin-Induced Exosome-like Extracellular Vesicles Contain Enhanced Levels of Sulfated Glycosaminoglycans which Facilitate the Interaction with Very Small Superparamagnetic Iron Oxide Particles.International journal of molecular sciences · 2023Article
- Extracellular Vesicles in Breast Cancer: From Biology and Function to Clinical Diagnosis and Therapeutic Management.International journal of molecular sciences · 2023Review
- Pathophysiology of Coagulation and Emerging Roles for Extracellular Vesicles in Coagulation Cascades and Disorders.Journal of clinical medicine · 2022Review
- Role of extracellular vesicles in severe pneumonia and sepsis.Expert opinion on biological therapy · 2022Review
- EVOO Promotes a Less Atherogenic Profile Than Sunflower Oil in Smooth Muscle Cells Through the Extracellular Vesicles Secreted by Endothelial Cells.Frontiers in nutrition · 2022Article
- Ectosome biogenesis and release processes observed by using live-cell dynamic imaging in mammalian glial cells.Quantitative imaging in medicine and surgery · 2021Article
- Extracellular Vesicles and Thrombosis: Update on the Clinical and Experimental Evidence.International journal of molecular sciences · 2021Review
- Factor VIIa Regulates the Level of Cell-Surface Tissue Factor through Separate but Cooperative Mechanisms.Cancers · 2021Article
- Uraemic extracellular vesicles augment osteogenic transdifferentiation of vascular smooth muscle cells via enhanced AKT signalling and PiT-1 expression.Journal of cellular and molecular medicine · 2021Article
- Extracellular Vesicles and Alveolar Epithelial-Capillary Barrier Disruption in Acute Respiratory Distress Syndrome: Pathophysiological Role and Therapeutic Potential.Frontiers in physiology · 2021Review
- Extracellular Vesicles for the Treatment of Radiation Injuries.Frontiers in pharmacology · 2021Review
- Endothelial cell-derived extracellular vesicles alter vascular smooth muscle cell phenotype through high-mobility group box proteins.Journal of extracellular vesicles · 2020Article
- Intercellular Communication by Vascular Endothelial Cell-Derived Extracellular Vesicles and Their MicroRNAs in Respiratory Diseases.Frontiers in molecular biosciences · 2020Review
- Review
- Extracellular vesicles: mediators and biomarkers of pathology along CNS barriers.Fluids and barriers of the CNS · 2018Review
- Endocytosis of Red Blood Cell Microparticles by Pulmonary Endothelial Cells is Mediated By Rab5.Shock (Augusta, Ga.) · 2018Article
- Endothelial Extracellular Vesicles in Pulmonary Function and Disease.Current topics in membranes · 2018Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Microparticles (MPs) are small membrane fragments shed from normal as well as activated, apoptotic or injured cells. Emerging evidence implicates MPs as a causal and/or contributing factor in altering normal vascular cell phenotype through initiation of proinflammatory signal transduction events and paracrine delivery of proteins, mRNA and miRNA. However, little is known regarding the mechanism by which MPs influence these events. Caveolae are important membrane microdomains that function as centers of signal transduction and endocytosis. Here, we tested the concept that the MP-induced pro-inflammatory phenotype shift in endothelial cells (ECs) depends on caveolae. Consistent with previous reports, MP challenge activated ECs as evidenced by upregulation of intracellular adhesion molecule-1 (ICAM-1) expression. ICAM-1 upregulation was mediated by activation of NF-κB, Poly [ADP-ribose] polymerase 1 (PARP-1) and the epidermal growth factor receptor (EGFR). This response was absent in ECs lacking caveolin-1/caveolae. To test whether caveolae-mediated endocytosis, a dynamin-2 dependent process, is a feature of the proinflammatory response, EC's were pretreated with the dynamin-2 inhibitor dynasore. Similar to observations in cells lacking caveolin-1, inhibition of endocytosis significantly attenuated MPs effects including, EGFR phosphorylation, activation of NF-κB and upregulation of ICAM-1 expression. Thus, our results indicate that caveolae play a role in mediating the pro-inflammatory signaling pathways which lead to EC activation in response to MPs.
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