{"created":"2024-10-29T00:33:29.276035+00:00","id":2006463,"links":{},"metadata":{"_buckets":{"deposit":"2aa08f5c-730c-4e9b-b175-360f1a43dad4"},"_deposit":{"created_by":7,"id":"2006463","owners":[7],"pid":{"revision_id":0,"type":"depid","value":"2006463"},"status":"published"},"_oai":{"id":"oai:tokushima-u.repo.nii.ac.jp:02006463","sets":["1713853213384:1713853296295:1716267877313:1716268556148"]},"author_link":["674","1251","599","323"],"item_10001_alternative_title_1":{"attribute_name":"タイトル別表記","attribute_value_mlt":[{"subitem_alternative_title":"破骨細胞におけるNF-κB活性化によるFas / S1P1クロストークがマウスTMJ関節炎の骨リモデリングを制御する","subitem_alternative_title_language":"ja"}]},"item_10001_biblio_info_7":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2017-07-04","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"4","bibliographicPageEnd":"1281","bibliographicPageStart":"1274","bibliographicVolumeNumber":"490","bibliographic_titles":[{"bibliographic_title":"Biochemical and Biophysical Research Communications","bibliographic_titleLang":"en"}]}]},"item_10001_description_5":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Enhanced turnover of subchondral trabecular bone is a hallmark of rheumatoid arthritis (RA) and it results from an imbalance between bone resorption and bone formation activities. To investigate the formation and activation of osteoclasts which mediate bone resorption, a Fas-deficient MRL/lpr mouse model which spontaneously develops autoimmune arthritis and exhibits decreased bone mass was studied. Various assays were performed on subchondral trabecular bone of the temporomandibular joint (TMJ) from MRL/lpr mice and MRL+/+ mice. Initially, greater osteoclast production was observed in vitro from bone marrow macrophages obtained from MRL/lpr mice due to enhanced phosphorylation of NF-kB, as well as Akt and MAPK, to receptor activator of nuclear factor-kB ligand (RANKL). Expression of sphingosine 1-phosphate receptor 1 (S1P1) was also significantly upregulated in the condylar cartilage. S1P1 was found to be required for S1P-induced migration of osteoclast precursor cells and downstream signaling via Rac1. When SN50, a synthetic NF-kB-inhibitory peptide, was applied to the MRL/lpr mice, subchondral trabecular bone loss was reduced and both production of osteoclastogenesis markers and sphingosine kinase (Sphk) 1/S1P1 signaling were reduced. Thus, the present results suggest that Fas/S1P1 signaling via activation of NF-kB in osteoclast precursor cells is a key factor in the pathogenesis of RA in the TMJ.","subitem_description_language":"en","subitem_description_type":"Abstract"}]},"item_10001_publisher_8":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"Elsevier 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