中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Staphylococcal enterotoxin C2 promotes osteogenesis and suppresses osteoclastogenesis of human mesenchymal stem cells

文献类型:期刊论文

作者Wei-ming Fu; Xiao Zhu; Hua Wang; Wei-mao Wang; Ju-yu Chen; Yan Liang; Jin-fang Zhang; Hsiang-fu Kung
刊名EXPERIMENTAL CELL RESEARCH
出版日期2014
英文摘要As a super-antigen, staphylococcal enterotoxin C2 (SEC2) stimulates the release of massive inflammatory cytokines such as interferon-gamma (IFN-gamma), interleukin-1 (IL-1) and interleukin-2 (IL-2) which are documented to implicate osteoblast differentiation. In the present study, SEC2 was found to significantly improve the osteoblast differentiation by up-regulating BMP2 and Runx2/Cbfa1 expression. Interferon (IFN)-inducible gene IFI16, a co-activator of Runx2/Cbfa1, was also activated by SEC2 in the osteoblast differentiation. In addition, exogenous introduction of SEC2 stimulated OPG expression and suppressed RANK!, suggesting suppression of osteoclastogenesis in hMSCs. Therefore, our results displayed that SEC2 plays an important role in the commitment of MSC to the osteoblast and it might be a potential new therapeutic candidate for bone regeneration.
收录类别SCI
原文出处http://www.sciencedirect.com/science/article/pii/S0014482713005259
语种英语
源URL[http://ir.siat.ac.cn:8080/handle/172644/6231]  
专题深圳先进技术研究院_南沙所
作者单位EXPERIMENTAL CELL RESEARCH
推荐引用方式
GB/T 7714
Wei-ming Fu,Xiao Zhu,Hua Wang,et al. Staphylococcal enterotoxin C2 promotes osteogenesis and suppresses osteoclastogenesis of human mesenchymal stem cells[J]. EXPERIMENTAL CELL RESEARCH,2014.
APA Wei-ming Fu.,Xiao Zhu.,Hua Wang.,Wei-mao Wang.,Ju-yu Chen.,...&Hsiang-fu Kung.(2014).Staphylococcal enterotoxin C2 promotes osteogenesis and suppresses osteoclastogenesis of human mesenchymal stem cells.EXPERIMENTAL CELL RESEARCH.
MLA Wei-ming Fu,et al."Staphylococcal enterotoxin C2 promotes osteogenesis and suppresses osteoclastogenesis of human mesenchymal stem cells".EXPERIMENTAL CELL RESEARCH (2014).

入库方式: OAI收割

来源:深圳先进技术研究院

浏览0
下载0
收藏0
其他版本

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。