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dc.contributor.authorZulueta, Aidaes_ES
dc.contributor.authorCaretti, Annaes_ES
dc.contributor.authorCampisi, Giuseppe Matteoes_ES
dc.contributor.authorBrizzolari, Andreaes_ES
dc.contributor.authorAbad, José Luises_ES
dc.contributor.authorParoni, R.es_ES
dc.contributor.authorSignorelli, Paolaes_ES
dc.contributor.authorGhidoni, Riccardoes_ES
dc.date.accessioned2017-06-23T08:42:05Z-
dc.date.available2017-06-23T08:42:05Z-
dc.date.issued2017-07-01-
dc.identifier.citationNaunyn Schmiedeberg's Archives of Pharmacology 390 (7): 753-759 (2017)es_ES
dc.identifier.urihttp://hdl.handle.net/10261/151893-
dc.description.abstractExposure to cigarette smoke represents the most important risk factor for the development of chronic obstructive pulmonary disease (COPD). COPD is characterized by chronic inflammation of the airways, imbalance of proteolytic activity resulting in the destruction of lung parenchyma, alveolar hypoxia, oxidative stress, and apoptosis. Sphingolipids are structural membrane components whose metabolism is altered during stress. Known as apoptosis and inflammation inducer, the sphingolipid ceramide was found to accumulate in COPD airways and its plasma concentration increased as well. The present study investigates the role of sphingolipids in the cigarette smoke-induced damage of human airway epithelial cells. Lung epithelial cells were pre-treated with sphingolipid synthesis inhibitors (myriocin or XM462) and then exposed to a mixture of nicotine, acrolein, formaldehyde, and acetaldehyde, the major toxic cigarette smoke components. The inflammatory and proteolytic responses were investigated by analysis of the mRNA expression (RT-PCR) of cytokines IL-1β and IL-8, and matrix metalloproteinase-9 and of the protein expression (ELISA) of IL-8. Ceramide intracellular amounts were measured by LC-MS technique. Ferric-reducing antioxidant power test and superoxide anion radical scavenging activity assay were used to assess the antioxidant power of the inhibitors of ceramide synthesis. We here show that ceramide synthesis is enhanced under treatment with a cigarette smoke mixture correlating with increased expression of inflammatory cytokines and matrix metalloproteinase 9. The use of inhibitors of ceramide synthesis protected from smoke induced damages such as inflammation, oxidative stress, and proteolytic imbalance in airways epithelia. © 2017, Springer-Verlag Berlin Heidelberg.es_ES
dc.description.sponsorshipFinancial support from the Italian Cystic Fibrosis Research Foundation (Grant no. FFC20-2013) is acknowledged. We thank the Health Sciences Department, University of Milan, for the Post-Doctoral fellowship to support A. Zulueta and the PhD program in Molecular and Translational Medicine to support G.M. Campisi.es_ES
dc.language.isoenges_ES
dc.publisherSpringeres_ES
dc.relation.isversionofPostprintes_ES
dc.rightsopenAccessen_EN
dc.subjectCeramidees_ES
dc.subjectChronic obstructive pulmonary diseasees_ES
dc.subjectCigarette smokees_ES
dc.subjectInflammationes_ES
dc.subjectOxidative stresses_ES
dc.subjectSphingolipidses_ES
dc.titleInhibitors of ceramide de novo biosynthesis rescue damages induced by cigarette smoke in airways epitheliaes_ES
dc.typeartículoes_ES
dc.identifier.doi10.1007/s00210-017-1375-2-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversion10.1007/s00210-017-1375-2es_ES
dc.embargo.terms2018-07-01es_ES
dc.relation.csices_ES
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item.cerifentitytypePublications-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextWith Fulltext-
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