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Increased RANKL-mediated osteoclastogenesis by interleukin-1β and endoplasmic reticulum stress : Increased RANKL-mediated osteoclastogenesis by interleukin-1 beta and endoplasmic reticulum stress
DC Field | Value | Language |
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dc.contributor.author | Lee, Eun-Gyeong | - |
dc.contributor.author | Sung, Myung-Soon | - |
dc.contributor.author | Yoo, Han-Gyul | - |
dc.contributor.author | Chae, Han-Jung | - |
dc.contributor.author | Kim, Hang-Rae | - |
dc.contributor.author | Yoo, Wan-Hee | - |
dc.date.accessioned | 2024-05-16T01:31:55Z | - |
dc.date.available | 2024-05-16T01:31:55Z | - |
dc.date.created | 2021-01-15 | - |
dc.date.created | 2021-01-15 | - |
dc.date.created | 2021-01-15 | - |
dc.date.created | 2021-01-15 | - |
dc.date.issued | 2014-12 | - |
dc.identifier.citation | Joint Bone Spine, Vol.81 No.6, pp.520-526 | - |
dc.identifier.issn | 1297-319X | - |
dc.identifier.uri | https://hdl.handle.net/10371/202634 | - |
dc.description.abstract | Objective: The mechanism by which IL-1 beta and thapsigargin (TG)-induced endoplasmic reticulum (ER) stress modulate the receptor activator of nuclear factor kappa-B ligand (RANKL)-mediated osteoclastogenesis remains elusive. Thus, we investigated the osteoclast-specific and ER signals in osteoclastogenesis of bone marrow-derived cells. Methods: Bone marrow cells (BMCs) were obtained from 5-week-old male ICR mice and cultured to be differentiated into osteoclasts with M-CSF and RANKL in the presence or absence of IL-1 beta, TG, or 4-phenylbutyric acid (PBA), an ER stress-reducing drug. The formation of osteoclasts was evaluated by tartrate-resistant acid phosphatase (TRAP) staining and resorption pit assay with a dentine slice. The molecular mechanism of IL-1 beta and ER stress in osteoclastogenesis was investigated in BMCs transfected with siRNA for GRP78, PERK and IRE1 using reverse transcription-polymerase chain reaction and immunoblotting for osteoclast-specific and ER stress signaling molecules. Results: IL-1 beta and ER stress induced by TG-augmented the formation of osteoclasts, which was significantly inhibited by PBA and was mediated with osteoclast-specific signals, including c-Fos, NFATc1, and ER stress-associated signaling pathways, such as PERK, IRE1, GRP78, and eIF2 alpha. siRNA-mediated knockdown of ER stress signals inhibited the expression of NFATc1 and c-Fos, thus reducing IL-1 beta and/or TG-induced formation of osteoclasts. Conclusions: Osteoclastogenesis by IL-1 beta and/or ER stress is mainly associated with upregulation of eIF2 alpha, GRP78, PERK and IRE1. These results suggest that the signaling pathway of ER stress-induced osteoclast formation might be a new therapeutic target to prevent inflammatory and destructive arthritic disease such as RA and diverse osteoporosis. (C) 2014 Societe francaise de rhumatologie. Published by Elsevier Masson SAS. All rights reserved. | - |
dc.language | 영어 | - |
dc.publisher | Elsevier Masson | - |
dc.title | Increased RANKL-mediated osteoclastogenesis by interleukin-1β and endoplasmic reticulum stress | - |
dc.title.alternative | Increased RANKL-mediated osteoclastogenesis by interleukin-1 beta and endoplasmic reticulum stress | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.jbspin.2014.04.012 | - |
dc.citation.journaltitle | Joint Bone Spine | - |
dc.identifier.wosid | 000346418700010 | - |
dc.identifier.scopusid | 2-s2.0-84922618793 | - |
dc.citation.endpage | 526 | - |
dc.citation.number | 6 | - |
dc.citation.startpage | 520 | - |
dc.citation.volume | 81 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Kim, Hang-Rae | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | UNFOLDED-PROTEIN RESPONSE | - |
dc.subject.keywordPlus | TUMOR-NECROSIS-FACTOR | - |
dc.subject.keywordPlus | RHEUMATOID-ARTHRITIS | - |
dc.subject.keywordPlus | ER STRESS | - |
dc.subject.keywordPlus | PRECURSOR DIFFERENTIATION | - |
dc.subject.keywordPlus | SYNOVIAL FIBROBLASTS | - |
dc.subject.keywordPlus | IMMUNE-SYSTEM | - |
dc.subject.keywordPlus | RECEPTOR | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordAuthor | Endoplasmic reticulum stress | - |
dc.subject.keywordAuthor | IL-1 beta | - |
dc.subject.keywordAuthor | Osteoclast | - |
dc.subject.keywordAuthor | 4-phenylbutyric acid | - |
dc.subject.keywordAuthor | Thapsigargin | - |
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