dc.contributor |
Universitat de Barcelona |
dc.contributor.author |
García-García, Francesc Josep |
dc.contributor.author |
Mullol i Miret, Joaquim |
dc.contributor.author |
Pérez-González, Maria |
dc.contributor.author |
Pujols Tarrés, Laura |
dc.contributor.author |
Alobid, Isam |
dc.contributor.author |
Roca i Ferrer, Jordi |
dc.contributor.author |
Picado Vallés, César |
dc.date |
2018-10-04T15:24:52Z |
dc.date |
2018-10-04T15:24:52Z |
dc.date |
2012-12-11 |
dc.date |
2018-10-04T15:24:52Z |
dc.identifier.citation |
1932-6203 |
dc.identifier.citation |
619973 |
dc.identifier.uri |
http://hdl.handle.net/2445/125068 |
dc.format |
8 p. |
dc.format |
application/pdf |
dc.language.iso |
eng |
dc.publisher |
Public Library of Science (PLoS) |
dc.relation |
Reproducció del document publicat a: https://doi.org/10.1371/journal.pone.0051281 |
dc.relation |
PLoS One, 2012, vol. 7, num. 12, p. e51281 |
dc.relation |
https://doi.org/10.1371/journal.pone.0051281 |
dc.rights |
cc-by (c) García-García, Francesc Josep et al., 2012 |
dc.rights |
info:eu-repo/semantics/openAccess |
dc.rights |
http://creativecommons.org/licenses/by/3.0/es |
dc.subject |
Asma |
dc.subject |
Aspirina |
dc.subject |
Transducció de senyal cel·lular |
dc.subject |
Asthma |
dc.subject |
Aspirin |
dc.subject |
Cellular signal transduction |
dc.title |
Signal transduction pathways (MAPKS, NF-kB, and C/EBP) regulating COX-2 expression in nasal fibroblasts from asthma patients with aspirin intolerance |
dc.type |
info:eu-repo/semantics/article |
dc.type |
info:eu-repo/semantics/publishedVersion |
dc.description.abstract |
Background Recent studies have revealed that cyclooxygenase-2 (COX-2) expression is down-regulated in aspirin-induced asthma (AIA). Various signal pathways (MAPKs, NF-κB and C/EBP) are involved in COX-2 regulation. Objective To investigate the regulation of COX-2 expression through MAP-kinase pathway activation and nuclear factor translocation in aspirin-induced asthma (AIA). Methods Fibroblasts were isolated from specimens of nasal mucosa (NM, N = 5) and nasal polyps (NP, N = 5). After IL-1β (1 ng/ml) incubation, COX-2 and phosphorylated forms of ERK, JNK and p38 MAPK were measured by Western blot. MAPK's role in IL-1β-induced COX-2 expression was assessed by treating cells with ERK (PD98059), JNK (SP600125) and p38 MAPK (SB203580) inhibitors (0.1-10 µM) prior to IL-1β exposure. NF-κB and C/EBP nuclear translocation was measured by Western blot and TransAM® after IL-1β (10 ng/ml) exposure. Results No differences were observed in the MAPK phosphorylation time-course between NM and NP-AIA fibroblasts. The p38 MAPK inhibitor at 10 µM significantly reduced IL-1β-induced COX-2 expression in NM fibroblasts (85%). In NP-AIA fibroblasts the COX-2 inhibition (65%) at 1 and 10 µM was not statistically significant compared to non-treated cells. ERK and JNK inhibitors had no significant effect in either the NM or NP-AIA cultures. The effect of IL-1β on NF-κB and C/EBP subunits' nuclear translocation was similar between NM and NP-AIA fibroblasts. Conclusions These results suggest that p38 MAPK is the only MAPK involved in IL-1β-induced COX-2 expression. NM and NP-AIA fibroblasts have similar MAPK phosphorylation dynamics and nuclear factor translocation (NF-κB and C/EBP). COX-2 downregulation observed in AIA patients appears not to be caused by differences in MAPK dynamics or transcription factor translocation. |