000147852 001__ 147852
000147852 005__ 20250108101618.0
000147852 0247_ $$2doi$$a10.3390/ijms22115604
000147852 0248_ $$2sideral$$a141363
000147852 037__ $$aART-2021-141363
000147852 041__ $$aeng
000147852 100__ $$aSanz-Rubio, David
000147852 245__ $$aCell-Selective Altered Cargo Properties of Extracellular Vesicles Following In Vitro Exposures to Intermittent Hypoxia
000147852 260__ $$c2021
000147852 5060_ $$aAccess copy available to the general public$$fUnrestricted
000147852 5203_ $$aIntermittent hypoxia (IH), a hallmark of obstructive sleep apnea (OSA), is associated with cardiovascular and metabolic dysfunction. However, the mechanisms underlying these morbidities remain poorly delineated. Extracellular vesicles (EVs) mediate intercellular communications, play pivotal roles in a multitude of physiological and pathological processes, and could mediate IH-induced cellular effects. Here, the effects of IH on human primary cells and the release of EVs were examined. Microvascular endothelial cells (HMVEC-d), THP1 monocytes, THP1 macrophages M0, THP1 macrophages M1, THP1 macrophages M2, pre-adipocytes, and differentiated adipocytes (HAd) were exposed to either room air (RA) or IH for 24 h. Secreted EVs were isolated and characterized using transmission electron microscopy, nanoparticle tracking analysis, and Western blotting. The effects of each of the cell-derived EVs on endothelial cell (EC) monolayer barrier integrity, on naïve THP1 macrophage polarity, and on adipocyte insulin sensitivity were also evaluated. IH did not alter EVs cell quantal release, but IH-EVs derived from HMVEC-d (p < 0.01), THP1 M0 (p < 0.01) and HAd (p < 0.05) significantly disrupted HMVEC-d monolayer integrity, particularly after H2O2 pre-conditioning. IH-EVs from HMVEC-d and THP1 M0 elicited M2-polarity changes did not alter insulin sensitivity responses. IH induces cell-selective changes in EVs cargo, which primarily seem to target the emergence of endothelial dysfunction. Thus, changes in EVs cargo from selected cell sources in vivo may play causal roles in some of the adverse outcomes associated with OSA.
000147852 536__ $$9info:eu-repo/grantAgreement/ES/ISCIII-FEDER-FIS/PI18-01524
000147852 540__ $$9info:eu-repo/semantics/openAccess$$aby$$uhttp://creativecommons.org/licenses/by/3.0/es/
000147852 590__ $$a6.208$$b2021
000147852 591__ $$aBIOCHEMISTRY & MOLECULAR BIOLOGY$$b69 / 297 = 0.232$$c2021$$dQ1$$eT1
000147852 591__ $$aCHEMISTRY, MULTIDISCIPLINARY$$b50 / 179 = 0.279$$c2021$$dQ2$$eT1
000147852 592__ $$a1.176$$b2021
000147852 593__ $$aComputer Science Applications$$c2021$$dQ1
000147852 593__ $$aInorganic Chemistry$$c2021$$dQ1
000147852 593__ $$aSpectroscopy$$c2021$$dQ1
000147852 593__ $$aOrganic Chemistry$$c2021$$dQ1
000147852 593__ $$aPhysical and Theoretical Chemistry$$c2021$$dQ1
000147852 593__ $$aMolecular Biology$$c2021$$dQ1
000147852 594__ $$a6.9$$b2021
000147852 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000147852 700__ $$aKhalyfa, Abdelnaby
000147852 700__ $$aQiao, Zhuanhong
000147852 700__ $$aUllate, Jorge
000147852 700__ $$0(orcid)0000-0001-9096-2294$$aMarin, José M.$$uUniversidad de Zaragoza
000147852 700__ $$aKheirandish-Gozal, Leila
000147852 700__ $$aGozal, David
000147852 7102_ $$11007$$2610$$aUniversidad de Zaragoza$$bDpto. Medicina, Psiqu. y Derm.$$cArea Medicina
000147852 773__ $$g22, 11 (2021), 5604 [189 pp.]$$pInt. j. mol. sci.$$tInternational Journal of Molecular Sciences$$x1661-6596
000147852 8564_ $$s1107184$$uhttps://zaguan.unizar.es/record/147852/files/texto_completo.pdf$$yVersión publicada
000147852 8564_ $$s2814110$$uhttps://zaguan.unizar.es/record/147852/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000147852 909CO $$ooai:zaguan.unizar.es:147852$$particulos$$pdriver
000147852 951__ $$a2025-01-08-09:02:04
000147852 980__ $$aARTICLE