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dc.contributor.authorAntón-Pacheco, Juan L.
dc.contributor.authorUsategui, Alicia
dc.contributor.authorMartínez, Iván
dc.contributor.authorGarcía-Herrero, Carmen M.
dc.contributor.authorGamez, Antonio P.
dc.contributor.authorGrau, Montserrat
dc.contributor.authorMartínez Relimpio, Ana Mª
dc.contributor.authorRodríguez-Peralto, José L.
dc.contributor.authorPablos, José L.
dc.date.accessioned2016-11-24T12:57:04Z
dc.date.available2016-11-24T12:57:04Z
dc.date.issued2016
dc.identifier.issn1531-4995
dc.identifier.urihttp://hdl.handle.net/10641/1248
dc.description.abstractIntroduction/Objective: Acquired tracheal stenosis (ATS) is an unusual disease often secondary to prolonged mechanical trauma. ATS pathogenesis involves inflammation and subsequent fibrosis with narrowing of the tracheal lumen. TGF-β represents a pivotal factor in most fibrotic processes and therefore, a potential target in this context. The aim of this study is to analyze the role of TGF-β as a target for anti-fibrotic interventions in tracheal stenosis. Methods: Human stenotic tracheobronchial tissues from patients with benign airway stenosis and normal controls from pneumonectomy specimens were analyzed. Tracheal stenosis was induced in adult NZ rabbits by a circumferential thermal injury to the mucosa during open surgery and re-anastomosis. Rabbits were treated postoperatively with a peritracheal collagen sponge containing a TGF-β peptide antagonist (p17) or vehicle. Fibrosis was determined by Masson’s trichrome staining, and α-SMA+ Results: Human and rabbit stenotic tissues showed extensive submucosal fibrosis, characterized by significantly increased α-SMA myofibroblasts, CTGF and p-Smad2/3 expression by immunohistochemistry. + myofibroblasts and CTGF expression. In human stenotic lesions, increased p-Smad2/3+ nuclei were also observed. p17 treatment significantly reduced the fibrotic thickness as well as the density of α-SMA+ myofibroblasts and CTGF+ Conclusion: ATS is characterized by a TGF-β dependent fibrotic process but reduction of the fibrotic component by TGF-β1 antagonist therapy was not sufficient to improve tracheal narrowing, suggesting that fibrosis may not be the main contributor to luminal stenosis. cells in rabbit stenotic lesions but failed to improve the luminal area.spa
dc.language.isoengspa
dc.publisherLaryngoscopespa
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 España*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es/*
dc.subjectTracheal stenosisspa
dc.subjectTGF-β antagonistspa
dc.subjectAnimal modelspa
dc.titleTGF-β antagonist attenuates fibrosis but not luminal narrowing in experimental tracheal stenosis.spa
dc.typearticlespa
dc.description.versionpre-printspa
dc.rights.accessRightsopenAccessspa
dc.description.extent1304 KBspa


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