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dc.contributor.author정희경-
dc.date.accessioned2019-11-30T08:59:12Z-
dc.date.available2019-11-30T08:59:12Z-
dc.date.issued2017-09-
dc.identifier.citationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v. 491, no. 3, page. 787-793en_US
dc.identifier.issn0006-291X-
dc.identifier.issn1090-2104-
dc.identifier.urihttps://www.sciencedirect.com/science/article/pii/S0006291X17314298?via%3Dihub-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/115483-
dc.description.abstractThe main aim of this study are to explore the role of bone-derived cells (BdCs) in anIcylosing spondylitis (AS) and determine the underlying molecular mechanisms of IL-23 production. Primary BdCs were isolated from diced bone of facet joints obtained during surgery from seven AS patients and seven disease control (Ct) patients. Osteoblastic activity of BdCs was assessed by measuring their alkaline phosphatase activity and by alizarin red staining. Osteoblast and endoplasmic reticulum (ER) stress related genes were assessed by quantitative PCR, immunoblotting, immunofluorescence, and immunohistochemistry. In addition, expression of IL-23 in response to BIX (selective BIP inducer X)-induced ER stress was evaluated by qPCR and ELISA. Protein interaction and binding to IL-23 promoter were confirmed by Immunoprecipitation and Chromatin immunoprecipitation, respectively. Transcript levels of genes involved in osteoblast function, as well as of the ER stress marker were higher in the AS group than the Ct group, and elevated RUNX2, BiP and IL-23 expression were observed in the BdCs, serum, and bone biopsies from the AS group. BIX-induced ER stress stimulated osteoblastic activity and IL-23 secretion by upregulating RUNX2 expression. Furthermore, in AS BdCs, RUNX2 interacted with C/EBP beta to bind to IL-23 promoter and RUNX2 knockdown suppressed IL-23 secretion. These finding may provide a molecular mechanism involved in sustained ER stress in AS BdCs stimulates the activation of RUNX2 and C/EBP beta genes, leading to IL-23 production. (C) 2017 Elsevier Inc. All rights reserved.en_US
dc.description.sponsorshipWe thank Prof. Young Wha Koh (Department of Pathology, Ajou University School of Medicine, Suwon, Republic of Korea) for help in evaluating the histologic. This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT& Future (NRF-2016R1A2B4008606) and the Ministry of Education, Science and Technology (NRF-2013R1A1A2009617).en_US
dc.language.isoen_USen_US
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCEen_US
dc.subjectAnkylosing spondylitisen_US
dc.subjectBone-derived cellsen_US
dc.subjectER stressen_US
dc.subjectRUNX2en_US
dc.subjectIL-23en_US
dc.titleA novel role for bone-derived cells in ankylosing spondylitis: Focus on IL-23en_US
dc.typeArticleen_US
dc.relation.no3-
dc.relation.volume491-
dc.identifier.doi10.1016/j.bbrc.2017.07.079-
dc.relation.page787-793-
dc.relation.journalBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.contributor.googleauthorJo, Sungsin-
dc.contributor.googleauthorKoo, Bon San-
dc.contributor.googleauthorLee, Bitnara-
dc.contributor.googleauthorKwon, Eunji-
dc.contributor.googleauthorLee, Young Lim-
dc.contributor.googleauthorChung, Heekyoung-
dc.contributor.googleauthorSung, Il-Hoon-
dc.contributor.googleauthorPark, Ye-Soo-
dc.contributor.googleauthorKim, Tae-Hwan-
dc.relation.code2017001220-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF MEDICINE[S]-
dc.sector.departmentDEPARTMENT OF MEDICINE-
dc.identifier.pidhc2n-
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