Blood-derived extracellular vesicles isolated from healthy donors exposed to air pollution modulate in vitro endothelial cells behavior

• Published in: Scientific reports Vol. 10; no. 1; p. 20138
• Main Authors: Rota, Federica, Ferrari, Luca, Hoxha, Mirjam, Favero, Chiara, Antonioli, Rita, Pergoli, Laura, Greco, Maria Francesca, Mariani, Jacopo, Lazzari, Lorenza, Bollati, Valentina
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 18.11.2020
• Subjects: 692/499; 692/53; 704/172; Adult; Air Pollution - adverse effects; Antigens, CD - metabolism; Body Mass Index; Cells, Cultured; Endothelial Cells - cytology; Endothelial Cells - drug effects; Endothelium, Vascular - cytology; Endothelium, Vascular - drug effects; Extracellular Vesicles - chemistry; Extracellular Vesicles - pathology; Extracellular Vesicles - physiology; Female; Healthy Volunteers; Humanities and Social Sciences; Humans; Male; Middle Aged; multidisciplinary; Particulate Matter - toxicity; Science; Science (multidisciplinary)
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-020-77097-9

The release of Extracellular Vesicles (EVs) into the bloodstream is positively associated with Particulate Matter (PM) exposure, which is involved in endothelial dysfunction and related to increased risk of cardiovascular disease. Obesity modifies the effects of PM exposure on heart rate variability and markers of inflammation, oxidative stress, and acute phase response. We isolated and characterized plasmatic EVs from six healthy donors and confirmed a positive association with PM exposure. We stratified for Body Mass Index (BMI) and observed an increased release of CD61+ (platelets) and CD105+ (endothelium) derived-EVs after high PM level exposure in Normal Weight subjects (NW) and no significant variations in Overweight subjects (OW). We then investigated the ability to activate endothelial primary cells by plasmatic EVs after both high and low PM exposure. NW-high-PM EVs showed an increased endothelial activation, measured as CD105+/CD62e+ (activated endothelium) EVs ratio. On the contrary, cells treated with OW-high-PM EVs showed reduced endothelial activation. These results suggest the ability of NW plasmatic EVs to communicate to endothelial cells and promote the crosstalk between activated endothelium and peripheral cells. However, this capacity was lost in OW subjects. Our findings contribute to elucidate the role of EVs in endothelial activation after PM exposure.