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The extracellular signal-regulated kinase mitogen-activated protein kinase/ribosomal S6 protein kinase 1 cascade phosphorylates cAMP response element-binding protein to induce MUC5B gene expression via D-prostanoid receptor signaling.

DC Field Value Language
dc.contributor.author박보령-
dc.contributor.author신동민-
dc.contributor.author유정윤-
dc.contributor.author윤주헌-
dc.contributor.author윤호근-
dc.contributor.author이상남-
dc.contributor.author최연호-
dc.date.accessioned2014-12-20T16:59:30Z-
dc.date.available2014-12-20T16:59:30Z-
dc.date.issued2011-
dc.identifier.issn0021-9258-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/93763-
dc.description.abstractMucus hypersecretion is a prominent feature of respiratory diseases, and MUC5B is a major airway mucin. Mucin gene expression can be affected by inflammatory mediators, including prostaglandin (PG) D(2,) an inflammatory mediator synthesized by hematopoietic PGD synthase (H-PGDS). PGD(2) binds to either D-prostanoid receptor (DP1) or chemoattractant receptor homologous molecule expressed on T-helper type 2 cells (CRTH2). We investigated the mechanisms by which PGD(2) induces MUC5B gene expression in airway epithelial cells. Western blot analysis showed that H-PGDS was highly expressed in nasal polyps. Similar results were obtained for PGD(2) expression. In addition, we could clearly detect the expressions of both H-PGDS and DP1 in nasal epithelial cells but not CRTH2. We demonstrated that PGD(2) increased MUC5B gene expression in normal human nasal epithelial cells as well as in NCI-H292 cells in vitro. S5751, a DP1 antagonist, inhibited PGD(2)-induced MUC5B expression, whereas a CRTH2 antagonist (OC0459) did not. These data suggest that PGD(2) induced MUC5B expression via DP1. Pretreatment with extracellular signal-regulated kinase (ERK) inhibitor (PD98059) blocked both PGD(2)-induced ERK mitogen-activated protein kinase (MAPK) activation and MUC5B expression. Proximity ligation assays showed direct interaction between RSK1 and cAMP response element-binding protein (CREB). Stimulation with PGD(2) caused an increase in intracellular cAMP levels, whereas intracellular Ca(2+) did not have such an effect. PGD(2)-induced MUC5B mRNA levels were regulated by CREB via direct interaction with two cAMP-response element sites (-921/-914 and -900/-893). Finally, we demonstrated that PGD(2) can induce MUC5B overproduction via ERK MAPK/RSK1/CREB signaling and that DP1 receptor may have suppressive effects in controlling MUC5B overproduction in the airway.-
dc.description.statementOfResponsibilityopen-
dc.format.extent34199~34214-
dc.relation.isPartOfJOURNAL OF BIOLOGICAL CHEMISTRY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHCell Line-
dc.subject.MESHCyclic AMP/metabolism-
dc.subject.MESHCyclic AMP Response Element-Binding Protein/metabolism*-
dc.subject.MESHEnzyme Activation/drug effects-
dc.subject.MESHEnzyme Activation/physiology-
dc.subject.MESHEpithelial Cells/cytology-
dc.subject.MESHEpithelial Cells/metabolism*-
dc.subject.MESHExtracellular Signal-Regulated MAP Kinases/antagonists & inhibitors-
dc.subject.MESHExtracellular Signal-Regulated MAP Kinases/metabolism*-
dc.subject.MESHFlavonoids/pharmacology-
dc.subject.MESHGene Expression Regulation/drug effects-
dc.subject.MESHGene Expression Regulation/physiology*-
dc.subject.MESHHumans-
dc.subject.MESHIntramolecular Oxidoreductases/metabolism-
dc.subject.MESHLipocalins/metabolism-
dc.subject.MESHMAP Kinase Signaling System/drug effects-
dc.subject.MESHMAP Kinase Signaling System/physiology-
dc.subject.MESHMucin-5B/biosynthesis*-
dc.subject.MESHPhosphorylation/drug effects-
dc.subject.MESHPhosphorylation/physiology-
dc.subject.MESHProstaglandin D2/metabolism-
dc.subject.MESHReceptors, Immunologic/antagonists & inhibitors-
dc.subject.MESHReceptors, Immunologic/metabolism-
dc.subject.MESHReceptors, Prostaglandin/antagonists & inhibitors-
dc.subject.MESHReceptors, Prostaglandin/metabolism*-
dc.subject.MESHRespiratory Mucosa/cytology-
dc.subject.MESHRespiratory Mucosa/metabolism*-
dc.subject.MESHResponse Elements/physiology-
dc.subject.MESHRibosomal Protein S6 Kinases, 90-kDa/metabolism*-
dc.subject.MESHThiophenes/pharmacology-
dc.titleThe extracellular signal-regulated kinase mitogen-activated protein kinase/ribosomal S6 protein kinase 1 cascade phosphorylates cAMP response element-binding protein to induce MUC5B gene expression via D-prostanoid receptor signaling.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Otorhinolaryngology (이비인후과학)-
dc.contributor.googleauthorYeon Ho Choi-
dc.contributor.googleauthorSang-Nam Lee-
dc.contributor.googleauthorHiroki Aoyagi-
dc.contributor.googleauthorYasundo Yamasaki-
dc.contributor.googleauthorJung-Yoon Yoo-
dc.contributor.googleauthorBoryung Park-
dc.contributor.googleauthorDong Min Shin-
dc.contributor.googleauthorHo-Geun Yoon-
dc.contributor.googleauthorJoo-Heon Yoon-
dc.identifier.doi10.1074/jbc.M111.247684-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01481-
dc.contributor.localIdA02091-
dc.contributor.localIdA02604-
dc.contributor.localIdA02625-
dc.contributor.localIdA02813-
dc.contributor.localIdA04110-
dc.contributor.localIdA02502-
dc.relation.journalcodeJ01258-
dc.identifier.eissn1083-351X-
dc.identifier.pmid21832046-
dc.subject.keywordDP1-
dc.subject.keywordMUC5B-
dc.subject.keywordProstaglandin D2-
dc.contributor.alternativeNamePark, Bo Ryung-
dc.contributor.alternativeNameShin, Dong Min-
dc.contributor.alternativeNameYoo, Jung Yoon-
dc.contributor.alternativeNameYoon, Joo Heon-
dc.contributor.alternativeNameYoon, Ho Geun-
dc.contributor.alternativeNameLee, Sang Nam-
dc.contributor.alternativeNameChoi, Yeon Ho-
dc.contributor.affiliatedAuthorPark, Bo Ryung-
dc.contributor.affiliatedAuthorShin, Dong Min-
dc.contributor.affiliatedAuthorYoon, Joo Heon-
dc.contributor.affiliatedAuthorYoon, Ho Geun-
dc.contributor.affiliatedAuthorLee, Sang Nam-
dc.contributor.affiliatedAuthorChoi, Yeon Ho-
dc.contributor.affiliatedAuthorYoo, Jung Yoon-
dc.contributor.affiliatedAuthor유정윤-
dc.rights.accessRightsfree-
dc.citation.volume286-
dc.citation.number39-
dc.citation.startPage34199-
dc.citation.endPage34214-
dc.identifier.bibliographicCitationJOURNAL OF BIOLOGICAL CHEMISTRY, Vol.286(39) : 34199-34214, 2011-
dc.identifier.rimsid28447-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers

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