IL-17A inhibits osteoclast differentiation of RANKL-stimulated RAW264.7 cells by suppressing JNK phosphorylation and c-Fos expression

Persistent ID (NDL): info:ndljp/pid/12154586

Material type: 博士論文

Author: 野阪, 興

Publisher: 大阪歯科学会

Publication date: 2014-12-24

Material Format: Digital

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Name of awarding university/degree: 大阪歯科大学,博士（歯学）

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Note (General)：: Periodontitis is a chronic inflammatory disease characterized by alveolar bone resorption. Inflammation-mediated bone loss is a major cause of various...

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Material Type: 博士論文
Title: IL-17A inhibits osteoclast differentiation of RANKL-stimulated RAW264.7 cells by suppressing JNK phosphorylation and c-Fos expression
Author/Editor: 野阪, 興
Author Heading: 野阪, 興
Publication, Distribution, etc.: 大阪歯科学会
Publication Date: 2014-12-24
Publication Date (W3CDTF): 2014-12-24
Alternative Title: IL-17A は JNK リン酸化と c-Fos 発現を抑えることにより RANKL 刺激されたRAW264.7 細胞の破⾻細胞分化を抑制する
Degree grantor/type: 大阪歯科大学
Date Granted: 2014-12-24
Date Granted (W3CDTF): 2014-12-24
Dissertation Number: 乙第1590号
Degree Type: 博士（歯学）
Conferring No. (Dissertation): 乙第1590号
Text Language Code: eng
Subject Heading: Interleukin-17A (IL-17A)
Osteoclast differentiation
RAW264.7 cells
Target Audience: 一般
Note (General): Periodontitis is a chronic inflammatory disease characterized by alveolar bone resorption. Inflammation-mediated bone loss is a major cause of various bone diseases, such as chronic periodontitis, and is due to an imbalance in bone remodeling that favors resorption. This imbalance is caused by increased inflammatory cytokines. Interleukin-17A (IL-17A) is a proinflammatory cytokine that is mainly secreted by activated T cells. IL-17A stimulates osteoclastic bone resorption via osteoblasts by inducing the expression of the receptor activator of NF-kB ligand (RANKL). However, little is known about the direct effects of IL-17A on the osteoclast precursors. We confirmed that IL-17A suppresses the osteoclast differentiation of RAW264.7 cells in the presence of RANKL in a dose-dependent manner. We also found that treatment with SP 600125, a specific inhibitor of c-Jun N-terminal kinase (JNK), significantly inhibits the TRAP activity of RAW264.7 cells, which were stimulated by RANKL. In addition, we found that IL-17 A reduces the phosphorylation of JNK and expressions of c-Fos, which were increased by RANKL stimulation. These results suggest that IL-17A-induces inhibition of JNK phosphorylation and that expression of c-Fos may be one of the factors that suppresses the differentiation of osteoclast precursors into osteoclasts.
2014年度
Persistent ID (NDL): info:ndljp/pid/12154586
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Collection: 障害者向け資料
Collection (Materials For Handicapped People:1): テキストデータ
Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
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Acquisition Basis: 博士論文（自動収集）
Date Accepted (W3CDTF): 2022-03-06T04:54:00+09:00
Date Created (W3CDTF): 2016-06-20
Format (IMT): application/pdf
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Availability of remote photoduplication service: 可
Periodical Title (URI): http://id.nii.ac.jp/1392/00000019/
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