Lung myofibroblasts are characterized by down-regulated cyclooxygenase-2 and its main metabolite, prostaglandin E2.
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Lung myofibroblasts are characterized by down-regulated cyclooxygenase-2 and its main metabolite, prostaglandin E2.

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Lung myofibroblasts are characterized by down-regulated cyclooxygenase-2 and its main metabolite, prostaglandin E2.

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dc.contributor.author Gabasa, M.
dc.contributor.author Royo, D.
dc.contributor.author Molina-Molina, M.
dc.contributor.author Roca-Ferrer, J.
dc.contributor.author Pujols, L.
dc.contributor.author Picado, C.
dc.contributor.author Xaubet, Antoni
dc.contributor.author Pereda Cervera, Javier
dc.date.accessioned 2014-07-07T11:53:25Z
dc.date.available 2014-07-07T11:53:25Z
dc.date.issued 2013
dc.identifier.uri http://hdl.handle.net/10550/36980
dc.description.abstract Background: Prostaglandin E2 (PGE2), the main metabolite of cyclooxygenase (COX), is a well-known anti-fibrotic agent. Moreover, myofibroblasts expressing a-smooth muscle actin (a-SMA), fibroblast expansion and epithelial-mesenchymal transition (EMT) are critical to the pathogenesis of idiopathic pulmonary fibrosis (IPF). Our aim was to investigate the expression of COX-2 and PGE2 in human lung myofibroblasts and establish whether fibroblast-myofibroblast transition (FMT) and EMT are associated with COX-2 and PGE2 down-regulation. Methods: Fibroblasts obtained from IPF patients (n = 6) and patients undergoing spontaneous pneumothorax (control,n = 6) and alveolar epithelial cell line A549 were incubated with TGF-b1 and FMT and EMT markers were evaluated. COX-2 and a-SMA expression, PGE2 secretion and cell proliferation were measured after IL-1b and PGE2 incubation. Results: Myofibroblasts from both control and IPF fibroblast cultures stimulated with IL-1b showed no COX-2 expression. IPF fibroblasts showed increased myofibroblast population and reduced COX-2 expression in response to IL-1b. TGF-b1 increased the number of myofibroblasts in a time-dependent manner. In contrast, TGF-b1 induced slight COX-2 expression at 4 h (without increase in myofibroblasts) and 24 h, but not at 72 h. Both IPF and control cultures incubated with TGF-b1 for 72 h showed diminished COX-2 induction, PGE2 secretion and a-SMA expression after IL-1b addition. The latter decreased proliferation in fibroblasts but not in myofibroblasts. A549 cells incubated with TGF-b1 for 72 h showed downregulated COX-2 expression and low basal PGE2 secretion in response to IL-1b. Immuno-histochemical analysis of IPF lung tissue showed no COX-2 immuno-reactivity in myofibroblast foci. Conclusions: Myofibroblasts are associated with COX-2 down-regulation and reduced PGE2 production, which could be crucial in IPF development and progression.
dc.language.iso eng
dc.relation.ispartof Plos One, 2013
dc.rights.uri info:eu-repo/semantics/openAccess
dc.source Gabasa M Royo D Molina-Molina M Roca-Ferrer J Pujols L Picado C Xaubet A Pereda Cervera, Javier 2013 Lung myofibroblasts are characterized by down-regulated cyclooxygenase-2 and its main metabolite, prostaglandin E2. Plos One
dc.subject Fisiologia cel·lular
dc.title Lung myofibroblasts are characterized by down-regulated cyclooxygenase-2 and its main metabolite, prostaglandin E2.
dc.type info:eu-repo/semantics/article
dc.date.updated 2014-07-07T11:53:25Z
dc.identifier.idgrec 089399

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