{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T03:18:47Z","timestamp":1790997527145,"version":"4.1.0"},"reference-count":43,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2024,8,2]],"date-time":"2024-08-02T00:00:00Z","timestamp":1722556800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2024,9]]},"abstract":"<jats:sec><jats:title>Abstract<\/jats:title><jats:p>The purpose of this study was to determine the effect of circulating microvesicles isolated from chronic electronic (e\u2010)cigarette users on cultured human umbilical vein endothelial cell (HUVEC) expression of nuclear factor\u2010\u03baB (NF\u2010\u03baB), cellular cytokine release, phosphorylation of endothelial nitric oxide synthase (eNOS) and NO production. The HUVECs were treated with microvesicles isolated via flow cytometry from nine non\u2010tobacco users (five male and four female; 22\u00a0\u00b1\u00a02\u00a0years of age) and 10 e\u2010cigarette users (six male and four female; 22\u00a0\u00b1\u00a02\u00a0years of age). Microvesicles from e\u2010cigarette users induced significantly greater release of interleukin\u20106 (183.4\u00a0\u00b1\u00a023.6\u00a0vs. 150.6\u00a0\u00b1\u00a015.4 pg\/mL; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.002) and interleukin\u20108 (160.0\u00a0\u00b1\u00a031.6\u00a0vs. 129.4\u00a0\u00b1\u00a011.2 pg\/mL; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.01), in addition to expression of p\u2010NF\u2010\u03baB p65 (Ser536) (18.8\u00a0\u00b1\u00a03.4 vs. 15.6\u00a0\u00b1\u00a01.5 a.u.; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.02) from HUVECs compared with microvesicles from non\u2010tobacco users. Nuclear factor\u2010\u03baB p65 was not significantly different between microvesicles from the non\u2010tobacco users and from the e\u2010cigarette users (87.6\u00a0\u00b1\u00a08.7\u00a0vs. 90.4\u00a0\u00b1\u00a024.6 a.u.; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.701). Neither total eNOS (71.4\u00a0\u00b1\u00a021.8\u00a0vs. 80.4\u00a0\u00b1\u00a024.5 a.u.; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.413) nor p\u2010eNOS (Thr495) (229.2\u00a0\u00b1\u00a026.5\u00a0vs. 222.1\u00a0\u00b1\u00a022.7 a.u.; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.542) was significantly different between microvesicle\u2010treated HUVECs from non\u2010tobacco users and e\u2010cigarette users. However, p\u2010eNOS (Ser1177) (28.9\u00a0\u00b1\u00a06.2\u00a0vs. 45.8\u00a0\u00b1\u00a09.0 a.u.; <jats:italic>P\u00a0<\/jats:italic>&lt;\u00a00.001) expression was significantly lower from e\u2010cigarette users compared with non\u2010tobacco users. Nitric oxide production was significantly lower (8.2\u00a0\u00b1\u00a00.6\u00a0vs. 9.7\u00a0\u00b1\u00a00.9\u00a0\u03bcmol\/L; <jats:italic>P<\/jats:italic>\u00a0=\u00a00.001) in HUVECs treated with microvesicles from e\u2010cigarette users compared with microvesicles from non\u2010tobacco users. This study demonstrated increased NF\u2010\u03baB activation and inflammatory cytokine production, in addition to diminished eNOS activity and NO production resulting from e\u2010cigarette use.<\/jats:p><\/jats:sec><jats:sec><jats:title>Highlights<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p><jats:bold>What is the central question of this study?<\/jats:bold><\/jats:p><jats:p>Circulating microvesicles contribute to cardiovascular health and disease via their effects on the vascular endothelium. The impact of electronic (e\u2010)cigarette use on circulating microvesicle phenotype is not well understood.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p><jats:bold>What is the main finding and its importance?<\/jats:bold><\/jats:p><jats:p>Circulating microvesicles from e\u2010cigarette users increase endothelial cell inflammation and impair endothelial nitric oxide production. Endothelial inflammation and diminished nitric oxide bioavailability are central factors underlying endothelial dysfunction and, in turn, cardiovascular disease risk. Deleterious changes in the functional phenotype of circulating microvesicles might contribute to the reported adverse effects of e\u2010cigarette use on cardiovascular health.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1113\/ep091715","type":"journal-article","created":{"date-parts":[[2024,8,2]],"date-time":"2024-08-02T12:49:13Z","timestamp":1722602953000},"page":"1593-1603","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Circulating extracellular microvesicles associated with electronic cigarette use increase endothelial cell inflammation and reduce nitric oxide production"],"prefix":"10.1113","volume":"109","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5616-5857","authenticated-orcid":false,"given":"Nicholas G.","family":"Evanoff","sequence":"first","affiliation":[{"name":"School of Kinesiology University of Minnesota  Minneapolis Minnesota USA"},{"name":"Center for Pediatric 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