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dc.contributor.author정일엽-
dc.date.accessioned2016-07-19T07:08:59Z-
dc.date.available2016-07-19T07:08:59Z-
dc.date.issued2015-01-
dc.identifier.citationIMMUNOLOGY, v. 144, Page. 79-90en_US
dc.identifier.issn0019-2805-
dc.identifier.issn1365-2567-
dc.identifier.urihttp://onlinelibrary.wiley.com/doi/10.1111/imm.12352/full-
dc.identifier.urihttp://hdl.handle.net/20.500.11754/22091-
dc.description.abstractAirway mucus hyperproduction is a common feature of chronic airway diseases such as severe asthma, chronic obstructive pulmonary disease and cystic fibrosis, which are closely associated with neutrophilic airway inflammation. S100A8, S100A9 and S100A12 are highly abundant proteins released by neutrophils and have been identified as important biomarkers in many inflammatory diseases. Herein, we report a new role for S100A8, S100A9 and S100A12 for producing MUC5AC, a major mucin protein in the respiratory tract. All three S100 proteins induced MUC5AC mRNA and the protein in normal human bronchial epithelial cells as well as NCI-H292 lung carcinoma cells in a dose-dependent manner. A Toll-like receptor 4 (TLR4) inhibitor almost completely abolished MUC5AC expression by all three S100 proteins, while neutralization of the receptor for advanced glycation end-products (RAGE) inhibited only S100A12-mediated production of MUC5AC. The S100 protein-mediated production of MUC5AC was inhibited by the pharmacological agents that block prominent signalling molecules for MUC5AC expression, such as mitogen-activated protein kinases, nuclear factor-B (NF-B) and epidermal growth factor receptor. S100A8, S100A9 and S100A12 equally elicited both phosphorylation of extracellular signal-regulated kinase (ERK) and nuclear translocation of NF-B/degradation of cytosolic IB with similar kinetics through TLR4. In contrast, S100A12 preferentially activated the ERK pathway rather than the NF-B pathway through RAGE. Collectively, these data reveal the capacity of these three S100 proteins to induce MUC5AC production in airway epithelial cells, suggesting that they all serve as key mediators linking neutrophil-dominant airway inflammation to mucin hyperproduction.en_US
dc.language.isoenen_US
dc.publisherWILEY-BLACKWELLen_US
dc.subjectairway epithelial cellsen_US
dc.subjectMUC5ACen_US
dc.subjectS100A12en_US
dc.subjectS100A8en_US
dc.subjectS100A9en_US
dc.titleS100A8, S100A9 and S100A12 activate airway epithelial cells to produce MUC5AC via extracellular signal-regulated kinase and nuclear factor-kappa B pathwaysen_US
dc.typeArticleen_US
dc.relation.volume144-
dc.identifier.doi10.1111/imm.12352-
dc.relation.page79-90-
dc.relation.journalIMMUNOLOGY-
dc.contributor.googleauthor정일엽-
dc.contributor.googleauthorChung, Il Yup-
dc.contributor.googleauthorKang, Jin Hyun-
dc.contributor.googleauthorHwang, Sae Mi-
dc.relation.code2015002698-
dc.sector.campusS-
dc.sector.daehakGRADUATE SCHOOL[S]-
dc.sector.departmentDEPARTMENT OF BIONANOTECHNOLOGY-
dc.identifier.pidiychu-
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GRADUATE SCHOOL[S](대학원) > BIONANOTECHNOLOGY(바이오나노학과) > Articles
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