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dc.contributor.authorRosas, Elisabet
dc.contributor.authorDreyfuss, Juliana L.
dc.contributor.authorMontell, Eulàlia
dc.contributor.authorVergés, Josep
dc.contributor.authorBalcells, Mercedes
dc.contributor.authorMelgar Lesmes, Pedro
dc.contributor.authorGarcia Polite, Fernando
dc.contributor.authorDel Rey Puech, Paula
dc.contributor.authorRosas, Elisabet Canyelles
dc.contributor.authorEdelman, Elazer R
dc.date.accessioned2017-12-14T20:07:33Z
dc.date.available2017-12-14T20:07:33Z
dc.date.issued2015-12
dc.date.submitted2015-12
dc.identifier.issn0021-9150
dc.identifier.urihttp://hdl.handle.net/1721.1/112764
dc.description.abstractBackground and aims: Osteoarthritic patients treated with high doses of chondroitin sulfate (CS) have a lower incidence of coronary heart disease - but the mechanistic aspects of these beneficial effects of CS remain undefined. We examined how CS treatment affects the formation of atheroma via interaction with endothelial cells and monocytes. Methods: We characterized arterial atheromatous plaques by multiphoton microscopy and serum pro-inflammatory cytokines by immunoenzymatic techniques in obese mice receiving CS (1 g/kg/day, i.p.) or vehicle for 6 days. Effects of CS on signaling pathways, cytokine secretion and macrophage migration were evaluated in cultures of human coronary endothelial cells and in a monocyte cell line stimulated with TNF-α by Western blot, immunoenzymatic techniques and transwell migration assays. Results: Treatment of obese mice with CS reduced the extension of foam cell coverage in atheromatous plaques of arterial bifurcations by 62.5%, the serum concentration of IL1β by 70%, TNF-α by 82% and selected chemokines by 25-35%. Cultures of coronary endothelial cells and monocytes stimulated with TNF-α secreted less pro-inflammatory cytokines in the presence of CS (P < 0.01). CS reduced the activation of the TNF-α signaling pathway in endothelial cells (pErk 36% of reduction, and NFκB 33% of reduction), and the migration of activated monocytes to inflamed endothelial cells in transwells (81 ± 6 vs. 13 ± 2, P < 0.001). Conclusions: CS interferes with the pro-inflammatory activation of monocytes and endothelial cells driven by TNF-α thus reducing the propagation of inflammation and preventing the formation of atherosclerotic plaques.en_US
dc.publisherElsevier BVen_US
dc.relation.isversionofhttp://dx.doi.org/10.1016/J.ATHEROSCLEROSIS.2015.12.016en_US
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivs Licenseen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en_US
dc.sourcePMCen_US
dc.titleTreatment with chondroitin sulfate to modulate inflammation and atherogenesis in obesityen_US
dc.typeArticleen_US
dc.identifier.citationMelgar-Lesmes, Pedro, et al. “Treatment with Chondroitin Sulfate to Modulate Inflammation and Atherogenesis in Obesity.” Atherosclerosis, vol. 245, Feb. 2016, pp. 82–87.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Institute for Medical Engineering & Scienceen_US
dc.contributor.departmentHarvard University--MIT Division of Health Sciences and Technologyen_US
dc.contributor.mitauthorMelgar Lesmes, Pedro
dc.contributor.mitauthorGarcia Polite, Fernando
dc.contributor.mitauthorDel Rey Puech, Paula
dc.contributor.mitauthorRosas, Elisabet Canyelles
dc.contributor.mitauthorEdelman, Elazer R
dc.relation.journalAtherosclerosisen_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.updated2017-12-14T17:21:33Z
dspace.orderedauthorsMelgar-Lesmes, Pedro; Garcia-Polite, Fernando; Del-Rey-Puech, Paula; Rosas, Elisabet; Dreyfuss, Juliana L.; Montell, Eulàlia; Vergés, Josep; Edelman, Elazer R.; Balcells, Mercedesen_US
dspace.embargo.termsNen_US
dc.identifier.orcidhttps://orcid.org/0000-0002-2009-5911
dc.identifier.orcidhttps://orcid.org/0000-0002-7832-7156
mit.licensePUBLISHER_CCen_US
mit.metadata.statusComplete


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