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学科主题: 临床医学
题名:
The aryl hydrocarbon receptor suppresses osteoblast proliferation and differentiation through the activation of the ERK signaling pathway
作者: 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
发表日期: 2014-11-01
DOI: 10.1016/j.taap.2014.08.025
卷: 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
所属项目编号: 2010CB529106 ; 31400767 ; 31370936
项目资助者: State Key Development Program for Basic Research of China ; National Nature Science Foundations of China
WOS记录号: WOS:000344980400012
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/66294
Appears in Collections:北京大学第二临床医学院_期刊论文

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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

Recommended Citation:
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.
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