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- W2891023273 abstract "Extracellular vesicles (EVs) are important carriers of biologic cargoes that mediate intercellular communication. As in other organs, EVs in the lung can convey proinflammatory signals that contribute to organ injury and disease, but they are also recognized to facilitate homeostatic crosstalk between alveolar macrophages and lung epithelial cells. Numerous chaperone proteins and cis-acting signals direct packaging of cargoes into EVs. Evidence suggests that components of the inflammatory milieu can promote loss of EV structural fidelity and cargo stability. Recent studies demonstrate that environmental toxins and endogenous molecules released during inflammation or injury influence EV uptake by lung epithelium. A better mechanistic understanding of EV cargo packaging, stability, and acquisition/utilization is necessary for optimizing therapeutic delivery of EVs in the lung. Extracellular vesicles (EVs) are increasingly appreciated as important vectors of information transmission between cells. Most research on EVs has emphasized their roles in inflammatory and pathologic conditions, and in the airways and alveoli, EV secretion by various cell types is implicated in various forms of lung disease. However, recent evidence also demonstrates a homeostatic role for lung EVs by mediating transmission of anti-inflammatory signals between alveolar macrophages and lung epithelial cells. Nevertheless, our understanding of the mechanisms responsible for EV cargo packaging, stability in the extracellular milieu, and acquisition by recipient cells remains limited. Here, we review the current understanding of these mechanistic aspects of vesicular communication and their potential modulation by constituents of the unique microenvironment of the lung. Extracellular vesicles (EVs) are increasingly appreciated as important vectors of information transmission between cells. Most research on EVs has emphasized their roles in inflammatory and pathologic conditions, and in the airways and alveoli, EV secretion by various cell types is implicated in various forms of lung disease. However, recent evidence also demonstrates a homeostatic role for lung EVs by mediating transmission of anti-inflammatory signals between alveolar macrophages and lung epithelial cells. Nevertheless, our understanding of the mechanisms responsible for EV cargo packaging, stability in the extracellular milieu, and acquisition by recipient cells remains limited. Here, we review the current understanding of these mechanistic aspects of vesicular communication and their potential modulation by constituents of the unique microenvironment of the lung. an adapter protein that is classically known to recruit ubiquitin-protein ligases to their specific substrates. ARRDC1 also promotes microvesicle biogenesis and packaging of cytosolic protein cargoes. elements present in the same biomolecule in which they exert their regulatory effects. the process of taking extracellular content into a cell by invagination of the plasma membrane to form a vacuolar compartment. a family of cytosolic proteins that participate in several cellular processes; these include facilitating biogenesis of, and recruiting ubiquitinated proteins into, multivesicular endosomes as well as promoting viral budding and other forms of cellular abscission. a class of multivesicular endosome-derived extracellular vesicles that are generated by exocytosis of intraluminal vesicles. Exos are enriched in endosomal proteins and represent the smallest type of extracellular vesicle, with an approximate diameter of 30–100 nm. a family of membrane-delimited structures that harbor diverse biologic cargoes, including lipids, proteins, and nucleic acids. Secreted by virtually every cell type in the body, EVs are important vehicles of information transmission among cells, both locally and distally. vesicles that form by membrane budding into the lumen of maturing multivesicular endosomes. artificial, lipid-enclosed spheres that are selectively engineered to encapsulate specific lipid, protein, or nucleic acid content. Administration of liposomes is gaining traction as a therapeutic tool for in vivo delivery of protective biomolecules. a class of extracellular vesicles (approximately 50–1000 nm in diameter) that arise via outward budding of the plasma membrane. MVs are enriched in cytosolic and plasma membrane-embedded proteins. intracellular organelles that take part in endocytic processes and give rise to exosomes. MVEs are formed via inward budding of the limiting membrane of an endosome. one of a variety of forms of covalent modification of a protein after its biosynthesis. unstable, oxygen-containing species that react with DNA, RNA, lipids, and proteins and that can promote cellular damage. a family of proteins that are induced by, and negatively regulate, cytokine-induced signaling pathways." @default.
- W2891023273 created "2018-09-27" @default.
- W2891023273 creator A5002841313 @default.
- W2891023273 creator A5084604101 @default.
- W2891023273 date "2018-11-01" @default.
- W2891023273 modified "2023-10-04" @default.
- W2891023273 title "Microenvironmental Influences on Extracellular Vesicle-Mediated Communication in the Lung" @default.
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- W2891023273 doi "https://doi.org/10.1016/j.molmed.2018.08.006" @default.
- W2891023273 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30244822" @default.
- W2891023273 hasPublicationYear "2018" @default.
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