IR@PKUHSC  > 北京大学第三临床医学院
学科主题临床医学
AG490 inhibits NFATc1 expression and STAT3 activation during RANKL induced osteoclastogenesis
Li, Chang-hong; Zhao, Jin-xia; Sun, Lin; Yao, Zhong-qiang; Deng, Xiao-li; Liu, Rui; Liu, Xiang-yuan
关键词Osteoclastogenesis Ag490 Rankl Nfatc1 Jak2/stat3
刊名BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
2013-06-14
DOI10.1016/j.bbrc.2013.04.084
435期:4页:533-539
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Biophysics
研究领域[WOS]Biochemistry & Molecular Biology ; Biophysics
关键词[WOS]OSTEOPROTEGERIN LIGAND ; RHEUMATOID-ARTHRITIS ; SIGNALING PATHWAYS ; NUCLEAR-FACTOR ; JAK INHIBITOR ; C-FOS ; DIFFERENTIATION ; CELLS ; IMMUNE ; OSTEOIMMUNOLOGY
英文摘要

Commonly, JAK/STAT relays cytokine signals for cell activation and proliferation, and recent studies have shown that the elevated expression of JAK/STAT is associated with the immune rejection of allografts and the inflammatory processes of autoimmune disease. However, the role which JAK2/STAT3 signaling plays in the receptor activator of nuclear factor-kappa B ligand (RANKL)-mediated osteoclastogenesis is unknown. In this study, we investigated the effects of AG490, specific JAK2 inhibitor, on osteoclast differentiation in vitro. AG490 significantly inhibited osteoclastogenesis in murine osteoclast precursor cell line RAW264.7 induced by RANKL. AG490 suppressed cell proliferation and delayed the G1 to S cell cycle transition. Furthermore, AG490 also suppressed the expression of nuclear factor of activated T cells (NFAT) c1 but not c-Fos in RAW264.7. Subsequently, we investigated various intracellular signaling components associated with osteoclastogenesis. AG490 had no effects on RANKL-induced activation of Akt, ERK1/2. Interestingly, AG490 partly inhibited RANKL-induced phosphorylation of Ser(727) in STAT3. Additionally, down-regulation of STAT3 using siRNA resulted in suppression of TRAP, RANK and NFATc1 expression. In conclusion, we demonstrated that AG490 inhibited RANKL-induced osteoclastogenesis by suppressing NFATc1 production and cell proliferation via the STAT3 pathway. These results suggest that inhibition of JAK2 may be useful for the treatment of bone diseases characterized by excessive osteoclastogenesis. (c) 2013 Elsevier Inc. All rights reserved.

语种英语
WOS记录号WOS:000321025800005
引用统计
被引频次:17[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56212
专题北京大学第三临床医学院
北京大学第三临床医学院_风湿免疫科
北京大学口腔医学院_综合治疗科
作者单位Peking Univ, Hosp 3, Dept Rheumatol & Immunol, Beijing 100191, Peoples R China
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GB/T 7714
Li, Chang-hong,Zhao, Jin-xia,Sun, Lin,et al. AG490 inhibits NFATc1 expression and STAT3 activation during RANKL induced osteoclastogenesis[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,2013,435(4):533-539.
APA Li, Chang-hong.,Zhao, Jin-xia.,Sun, Lin.,Yao, Zhong-qiang.,Deng, Xiao-li.,...&Liu, Xiang-yuan.(2013).AG490 inhibits NFATc1 expression and STAT3 activation during RANKL induced osteoclastogenesis.BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,435(4),533-539.
MLA Li, Chang-hong,et al."AG490 inhibits NFATc1 expression and STAT3 activation during RANKL induced osteoclastogenesis".BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 435.4(2013):533-539.
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