Dkk-1-TNF-alpha crosstalk regulates MC3T3E1 pre-osteoblast proliferation and differentiation under mechanical stress through the ERK signaling pathway

作者全名："Wu, Yeke; Jing, Zheng; Deng, Disi; Yan, Jin; Liu, Min; Li, Li; Zuo, Yuling; Wu, Wenbin; Hu, Qiongying; Xie, Yunfei"

作者地址："[Wu, Yeke; Zuo, Yuling] Hosp Chengdu Univ Tradit Chinese Med, Dept Stomatol, Chengdu, Peoples R China; [Jing, Zheng] Chongqing Med Univ, Coll Stomatol, Chongqing, Peoples R China; [Deng, Disi; Yan, Jin; Liu, Min] Hosp Chengdu Univ Tradit Chinese Med, Dept Gynaecol, Chengdu, Peoples R China; [Li, Li] Hosp Chengdu Univ Tradit Chinese Med, Dept Radiol, Chengdu, Peoples R China; [Wu, Wenbin] Hosp Chengdu Univ Tradit Chinese Med, Dept Geriatr, Chengdu, Peoples R China; [Hu, Qiongying] Hosp Chengdu Univ Tradit Chinese Med, Dept Lab Med, 39 Shierqiao Rd, Chengdu 610072, Peoples R China; [Xie, Yunfei] Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Dept Nucl Med, Chengdu 610072, Peoples R China"

通信作者："Hu, QY (通讯作者)，Hosp Chengdu Univ Tradit Chinese Med, Dept Lab Med, 39 Shierqiao Rd, Chengdu 610072, Peoples R China.; Xie, YF (通讯作者)，Univ Elect Sci & Technol China, Sichuan Prov Peoples Hosp, Dept Nucl Med, Chengdu 610072, Peoples R China."

来源：MOLECULAR AND CELLULAR BIOCHEMISTRY

ESI学科分类：MOLECULAR BIOLOGY & GENETICS

WOS号：WOS:000913809800001

JCR分区：Q3

影响因子：3.5

年份：2023

卷号：　

期号：　

开始页：　

结束页：　

文献类型：Article; Early Access

关键词：Mechanical stress; Pre-osteoblast; Dkk-1; TNF-alpha; ERK signaling pathway

摘要："The study aims to explore the role of the ERK signaling pathway in the crosstalk between Dkk-1 and TNF-alpha in MC3T3E1 pre-osteoblasts under cyclic tensile/compressive stress. A forced four-point bending system was used to apply cyclic uniaxial tensile/compressive strain (2000 mu, 0.5 Hz) to MC3T3E1 cells. Dkk-1 and TNF-alpha expression were upregulated in MC3T3E1 cells under compressive strain. Cell proliferation, the cell cycle, osteogenesis-related gene (Wnt5a, Runx2, Osterix) expression, beta-catenin expression, and the p-ERK/ERK ratio were significantly enhanced, whereas apoptosis, the RANKL/OPG ratio, and TNF-alpha expression were significantly attenuated, by Dkk-1 silencing. Dkk-1 expression increased and the effects of Dkk-1 silencing were reversed when exogenous TNF-alpha was added. Mechanically, TNF-alpha crosstalked with Dkk-1 through ERK signaling in MC3T3E1 cells. ERK signaling blockade impaired Dkk-1-induced TNF-alpha expression and TNF-alpha-mediated Dkk-1 expression. Dkk-1 and TNF-alpha crosstalked, partially through ERK signaling, in MC3T3E1 cells under compressive/tensile strain, synergistically modulating various biological behaviors of the cells. These findings not only provide mechanical insight into the cellular events and molecular regulation of orthodontic tooth movement (OTM), but also aid the development of novel strategies to accelerate OTM."

基金机构："National Nature Science Foundation of China [81973684, 81500818, 81873334, 82174358]"

基金资助正文："AcknowledgementsThis work was supported by grants from the National Nature Science Foundation of China (Nos. 81973684, 81500818, 81873334, and 82174358)."