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dc.contributor.authorMelgar Lesmes, Pedro
dc.contributor.authorSanchez Herrero, Alvaro
dc.contributor.authorLozano Juan, Ferran
dc.contributor.authorde la Torre Hernández, Jose
dc.contributor.authorMontell, Eulàlia
dc.contributor.authorJiménez, Wladimiro
dc.contributor.authorEdelman, Elazer R
dc.contributor.authorBalcells-Camps, Mercedes
dc.date.accessioned2020-07-23T19:25:30Z
dc.date.available2020-07-23T19:25:30Z
dc.date.issued2018-06
dc.identifier.issn0340-6245
dc.identifier.issn2567-689X
dc.identifier.urihttps://hdl.handle.net/1721.1/126361
dc.description.abstractChondroitin sulphate (CS) has long been used to treat osteoarthritis. Some investigations have also shown that the treatment with CS could reduce coronary events in patients with heart disease but no studies have identified the mechanistic role of these therapeutic effects. We aimed to investigate how the treatment with CS can interfere with the progress of atherosclerosis. The aortic arch, thoracic aorta and serum were obtained from apolipoprotein E (ApoE) knockout mice fed for 10 weeks with high-fat diet and then treated with CS (300 mg/kg, n = 15) or vehicle (n = 15) for 4 weeks. Atheromatous plaques were highlighted in aortas with Oil Red staining and analysed by microscopy. ApoE knockout mice treated with CS exhibited attenuated atheroma lesion size by 68% as compared with animals receiving vehicle. Serum lipids, glucose and C-reactive protein were not affected by treatment with CS. To investigate whether CS locally affects the inflamed endothelium or the formation of foam cells in plaques, human endothelial cells and monocytes were stimulated with tumour necrosis factor α or phorbol myristate acetate in the presence or absence of CS. CS reduced the expression of vascular cell adhesion molecule 1, intercellular adhesion molecule 1 and ephrin-B2 and improved the migration of inflamed endothelial cells. CS inhibited foam cell formation in vivo and concomitantly CD36 and CD146 expression and oxidized low-density lipoprotein uptake and accumulation in cultured activated human monocytes and macrophages. Reported cardioprotective effects of CS may arise from modulation of pro-inflammatory activation of endothelium and monocytes and foam cell formation.en_US
dc.language.isoen
dc.publisherGeorg Thieme Verlag KGen_US
dc.relation.isversionofhttp://dx.doi.org/10.1055/s-0038-1657753en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alikeen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/en_US
dc.sourcePMCen_US
dc.titleChondroitin Sulphate Attenuates Atherosclerosis in ApoE Knockout Mice Involving Cellular Regulation of the Inflammatory Responseen_US
dc.typeArticleen_US
dc.identifier.citationMelgar-Lesmes, Pedro et al. "Chondroitin Sulphate Attenuates Atherosclerosis in ApoE Knockout Mice Involving Cellular Regulation of the Inflammatory Response." Thrombosis and Haemostatis 118, 7 (June 2018): 1329-1339 © 2018 Georg Thieme Verlag KGen_US
dc.contributor.departmentMassachusetts Institute of Technology. Institute for Medical Engineering & Scienceen_US
dc.relation.journalThrombosis and Haemostatisen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dc.date.updated2019-10-09T17:48:22Z
dspace.date.submission2019-10-09T17:48:24Z
mit.journal.volume118en_US
mit.journal.issue07en_US
mit.metadata.statusComplete


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