Role of extracellular vesicles in cell-cell communication and inflammation following exposure to pulmonary toxicants. (February 2020)

• Record Type: Journal Article
• Authors: Andres, Jaclynn; Smith, Ley Cody; Murray, Alexa; Jin, Yang; Businaro, Rita; Laskin, Jeffrey D.; Laskin, Debra L.
• Is Part Of: Cytokine & growth factor reviews. Volume 51(2020)
• Page Start: 12
• Page End: 18
• Publication Date: 2020-02
• Subjects: ABs apoptotic bodies -- APOB apolipoprotein B -- APOLI apolipoprotein L1 -- BAL bronchoalveolar lavage fluid -- C1QA complement C1q A chain -- C1Qc complement C1q C chain -- C1S complement component -- CCN cellular communication network factor -- CETP cholesterol ester transfer protein -- CFB complement factor B -- CLU clusterin -- CTGF connective tissue growth factor -- DAMPs damage-associated molecular patterns -- EVs extracellular vesicles -- HMGB1 high mobility group box 1 -- ICAM intracellular adhesion molecule -- LPA lipoprotein A -- LPS lipopolysaccharide -- MIP macrophage inflammatory protein -- MMP matrix metalloproteinase -- MVs microvesicles -- NOV nephroblastoma overexpressed -- PBMC peripheral blood mononuclear cells -- PM particulate matter -- ROCK rho-associated protein kinase -- SAA4 serum amyloid A4 -- SERPINA5 serpin family A member 5 -- SOCS suppressor of cytokine signaling -- TF tissue factor -- TLR toll-like receptor -- TNF tumor necrosis factor -- Tsg tumor susceptibility gene; Macrophages -- Inflammation -- Epithelial cells -- Ozone -- Cigarette smoke -- Lipopolysaccharide; Cytokines -- Periodicals; 571.84
• DOI: 10.1016/j.cytogfr.2019.12.001
• Languages: English
• ISSNs: 1359-6101

Abstract

Highlights: Extracellar vesicles are released following exposure to pulmonary toxicants. Extracellular vesicles include exosomes, microvesicles and apoptotic bodies. Extracellular vesicles contribute to cell cell communication and inflammation. Extracellular vesicles contain cargo that mediate biological effects. Abstract: Extracellular vesicles (EVs) have emerged as key regulators of cell-cell communication during inflammatory responses to lung injury induced by diverse pulmonary toxicants including cigarette smoke, air pollutants, hyperoxia, acids, and endotoxin. Many lung cell types, including epithelial cells and endothelial cells, as well as infiltrating macrophages generate EVs. EVs appear to function by transporting cargo to recipient cells that, in most instances, promote their inflammatory activity. Biologically active cargo transported by EVs include miRNAs, cytokines/chemokines, damage-associated molecular patterns (DAMPs), tissue factor (TF)s, and caspases. Findings that EVs are taken up by target cells such as macrophages, and that this leads to increased proinflammatory functioning provide support for their role in the development of pathologies associated with toxicant exposure. Understanding the nature of EVs responding to toxic exposures and their cargo may lead to the development of novel therapeutic approaches to mitigating lung injury.