Fas/S1P1 crosstalk via NF-κB activation in osteoclasts controls subchondral bone remodeling in murine TMJ arthritis

• Material Type: 博士論文
• Title: Fas/S1P1 crosstalk via NF-κB activation in osteoclasts controls subchondral bone remodeling in murine TMJ arthritis
• Author/Editor: Hutami, Islamy Rahma; Izawa, Takashi; Mino-Oka, Akiko; Shinohara, Takehiro; Mori, Hiroki; Iwasa, Akihiko; Tanaka, Eiji
• Author Heading: Hutami, Islamy Rahma; Izawa, Takashi; Mino-Oka, Akiko; Shinohara, Takehiro; Mori, Hiroki; Iwasa, Akihiko; Tanaka, Eiji
• Publication, Distribution, etc.: Elsevier Inc.
• Publication Date: 2017-07-04
• Publication Date (W3CDTF): 2017-07-04
• 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
• Periodical title: Biochemical and Biophysical Research Communications
• No. or year of volume/issue: 490 4
• Volume: 490
• Issue: 4
• Pages: 1274-1281
• ISSN (Periodical Title): ISSN : 0006-291X; ISSN : 1090-2104
• Degree grantor/type: 徳島大学
• Date Granted: 2019-03-22
• Dissertation Number: 甲第3279号
• Degree Type: 博士（歯学）
• Text Language Code: eng
• Subject Heading: FAS; S1P1; OSTEOCLAST; TEMPOROMANDIBULAR JOINT; SN50
• Target Audience: 一般
• Note (General): 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.
• Format (IMT): application/pdf
• Source: comment：fulltext; http://repo.lib.tokushima-u.ac.jp/files/public/11/113368/20190607153200389751/k3279_abstract.pdf; http://repo.lib.tokushima-u.ac.jp/files/public/11/113368/20190607153201190022/k3279_review.pdf; http://repo.lib.tokushima-u.ac.jp/files/public/11/113368/20190607153201493910/k3279_fulltext.pdf
• Access Restrictions: インターネット公開
• Related Material (DOI): 10.1016/j.bbrc.2017.07.006
• Periodical Title (NCID): AA00564395; https://ci.nii.ac.jp/ncid/AA00564395; AA11542044; https://ci.nii.ac.jp/ncid/AA11542044
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 徳島大学 : 徳島大学機関リポジトリ