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The Regulatory Role of Rolipram on Inflammatory Mediators and Cholinergic/Adrenergic Stimulation-Induced Signals in Isolated Primary Mouse Submandibular Gland Cells

DC FieldValueLanguage
dc.contributor.author신동민-
dc.date.accessioned2017-02-24T08:19:24Z-
dc.date.available2017-02-24T08:19:24Z-
dc.date.issued2016-
dc.identifier.issn0962-9351-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/146626-
dc.description.abstractExposure to bacterial lipopolysaccharides (LPS) induces inflammatory signals in salivary glands. We investigated the regulatory role of phosphodiesterase 4 (PDE4) inhibitor rolipram on inflammatory mediators and cholinergic/adrenergic stimulation-induced intracellular Ca(2+) signaling in salivary acinar and ductal cells. Submandibular gland (SMG) expressed PDE4A through 4D mRNA and PDE4 was localized in the luminal membrane of SMG. LPS induced Ca(2+) signaling and ROS production in SMG. Treatment with rolipram blocked LPS-induced Ca(2+) increase and ROS production. The application of histamine evoked Ca(2+) signals and ROS production, which were attenuated by rolipram in SMG cells. Moreover, LPS-induced NLRP3 inflammasome and cleaved caspase-1 were inhibited by rolipram. The inhibitory role of rolipram in ROS-induced Ca(2+) signaling was mainly observed in acinar cells and not in ductal cells. Rolipram also protected SMG acinar but not ductal cells from LPS-induced cell membrane damage. In the case of cholinergic/adrenergic stimulation, carbachol/isoproterenol-induced Ca(2+) signals were upregulated by the treatment of rolipram in SMG. In the case of cAMP-dependent ductal bicarbonate secretion by rolipram, no effect was observed on the modulation of ductal chloride/bicarbonate exchange activity. Rolipram could suppress the inflammatory signals and could be a potential therapeutic strategy against LPS-induced inflammation to protect the salivary gland cells.-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.languageEnglish-
dc.publisherHindawi Pub. Corp.-
dc.relation.isPartOfMEDIATORS OF INFLAMMATION-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHCalcium Signaling/drug effects-
dc.subject.MESHCells, Cultured-
dc.subject.MESHHistamine/pharmacology-
dc.subject.MESHInflammation/metabolism*-
dc.subject.MESHLipopolysaccharides/pharmacology-
dc.subject.MESHMice-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.subject.MESHReverse Transcriptase Polymerase Chain Reaction-
dc.subject.MESHRolipram/pharmacology*-
dc.subject.MESHSignal Transduction/drug effects-
dc.subject.MESHSubmandibular Gland/drug effects*-
dc.subject.MESHSubmandibular Gland/metabolism*-
dc.titleThe Regulatory Role of Rolipram on Inflammatory Mediators and Cholinergic/Adrenergic Stimulation-Induced Signals in Isolated Primary Mouse Submandibular Gland Cells-
dc.typeArticle-
dc.publisher.locationUnited States-
dc.contributor.collegeCollege of Dentistry-
dc.contributor.departmentDept. of Oral Biology-
dc.contributor.googleauthorDong Un Lee-
dc.contributor.googleauthorDong Min Shin-
dc.contributor.googleauthorJeong Hee Hong-
dc.identifier.doi10.1155/2016/3745961-
dc.contributor.localIdA02091-
dc.relation.journalcodeJ02194-
dc.identifier.eissn1466-1861-
dc.identifier.pmid27143817-
dc.contributor.alternativeNameShin, Dong Min-
dc.contributor.affiliatedAuthorShin, Dong Min-
dc.citation.volume2016-
dc.citation.startPage3745961-
dc.identifier.bibliographicCitationMEDIATORS OF INFLAMMATION, Vol.2016 : 3745961, 2016-
dc.date.modified2017-02-24-
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers

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