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The aryl hydrocarbon receptor suppresses osteoblast proliferation and differentiation through the activation of the ERK signaling pathway
Yu, Haitao1; Du, Yuxuan1; Zhang, Xulong1; Sun, Ying1; Li, Shentao1; Dou, Yunpeng1; Li, Zhanguo2; Yuan, Huihui1; Zhao, Wenming1
关键词Aryl hydrocarbon receptor (Ahr) Rheumatoid arthritis (RA) Osteoblasts Proliferation Differentiation ERK signaling pathway
刊名TOXICOLOGY AND APPLIED PHARMACOLOGY
2014-11-01
DOI10.1016/j.taap.2014.08.025
280期:3页:502-510
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pharmacology & Pharmacy ; Toxicology
研究领域[WOS]Pharmacology & Pharmacy ; Toxicology
关键词[WOS]COLLAGEN-INDUCED ARTHRITIS ; RHEUMATOID-ARTHRITIS ; T-CELLS ; PROTEIN-KINASES ; BONE-RESORPTION ; TNF-ALPHA ; 2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN ; MICE ; INFLAMMATION ; GROWTH
英文摘要

Ahr activation is known to be associated with synovitis and exacerbated rheumatoid arthritis (RA), but its contributions to bone loss have not been completely elucidated. Osteoblast proliferation and differentiation are abnormal at the erosion site in RA. Here, we reported that the expression of Ahr was increased in the hind paws′ bone upon collagen-induced arthritis (CIA) in mice, and the levels of Ahr were negatively correlated with bone mineral density (BMD). In addition, immunofluorescent staining:showed that the high expression of Ahr was mainly localized in osteoblasts from the CIA mice compared to normal controls. Moreover, the luciferase intensity of Ahr in the nucleus increased by 12.5% in CIA osteoblasts compared to that in normal controls. In addition, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) activation of the Ahr inhibited pre-osteoblast MC3T3-E1 cellular proliferation and differentiation in a dose-dependent manner. Interestingly, the levels of alkaline phosphatase (ALP) mRNA expression in the osteoblasts of CIA mice were reduced compared to normal controls. In contrast, decreased ALP expression by activated Ahr was completely reversed after pretreatment with an Ahr inhibitor (CH-223191) in MC3T3-E1 cell lines and primary osteoblasts on day 5. Our data further showed that activation of Ahr promoted the phosphorylation of ERK after 5 days. Moreover, Ahr-dependent activation of the ERK signaling pathway decreased the levels of proliferation cells and inhibited ALP activity in MC3T3-E1 cells. These results demonstrated that the high expression of Ahr may suppress osteoblast proliferation and differentiation through activation of the ERK signaling pathway, further enabling bone erosion in CIA mice. (C) 2014 Elsevier Inc. All rights reserved.

语种英语
WOS记录号WOS:000344980400012
项目编号2010CB529106 ; 31400767 ; 31370936
资助机构State Key Development Program for Basic Research of China ; National Nature Science Foundations of China
引用统计
被引频次:16[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/400002259/66294
专题北京大学第二临床医学院
北京大学第二临床医学院_风湿免疫科
作者单位1.Capital Med Univ, Sch Basic Med Sci, Dept Immunol, Beijing 100069, Peoples R China
2.Peking Univ, Peoples Hosp, Clin Immunol Ctr, Dept Rheumatol & Immunol, Beijing 100044, Peoples R China
推荐引用方式
GB/T 7714
Yu, Haitao,Du, Yuxuan,Zhang, Xulong,et al. The aryl hydrocarbon receptor suppresses osteoblast proliferation and differentiation through the activation of the ERK signaling pathway[J]. TOXICOLOGY AND APPLIED PHARMACOLOGY,2014,280(3):502-510.
APA Yu, Haitao.,Du, Yuxuan.,Zhang, Xulong.,Sun, Ying.,Li, Shentao.,...&Zhao, Wenming.(2014).The aryl hydrocarbon receptor suppresses osteoblast proliferation and differentiation through the activation of the ERK signaling pathway.TOXICOLOGY AND APPLIED PHARMACOLOGY,280(3),502-510.
MLA Yu, Haitao,et al."The aryl hydrocarbon receptor suppresses osteoblast proliferation and differentiation through the activation of the ERK signaling pathway".TOXICOLOGY AND APPLIED PHARMACOLOGY 280.3(2014):502-510.
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