Suppression of Sclerostin and Dickkopf-1 levels in patients with fluorine bone injury

被引：15

作者：

Wang, Wenpeng ^{[1
]}

Xu, Jian ^{[1
]}

Liu, Kejian ^{[1
]}

Liu, Xiaoli ^{[1
]}

Li, Changcheng ^{[1
]}

Cui, Caiyan ^{[1
]}

Zhang, Yuzeng ^{[1
]}

Li, Huabing ^{[2
]}

机构：

[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Sch Publ Hlth, Minist Educ,Key Lab Environm & Hlth, Wuhan 430030, Peoples R China

[2] Ctr Dis Control & Prevent, Jianshi Country 445300, Hubei Province, Peoples R China

来源：

ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY | 2013年 / 35卷 / 03期

基金：

中国国家自然科学基金;

关键词：

Fluorine bone injury; Sclerostin; Dickkopf-1; Fluoride; ENDEMIC FLUOROSIS; MINERAL DENSITY; SOST GENE; DISEASE; ELEVATION; CATENIN; SERUM; RATS;

D O I：

10.1016/j.etap.2013.01.005

中图分类号：

X [环境科学、安全科学];

学科分类号：

08 ; 0830 ;

摘要：

Evidence has been accumulating for the role of Sclerostin and Dickkopf-1 as the antagonists of Wnt/beta-Catenin signaling pathway, which suppresses bone formation through inhibiting osteoblastic function. To get deep-inside information about the expression of the antagonists in patients with fluorine bone injury, a case-control study was conducted in two counties in Hubei Province. Urinary and serum fluoride were significantly higher in patients with fluorine bone injury than in healthy controls. Additionally, patients with fluorine bone injury had significantly lower serum Sclerostin and Dickkopf-1 levels compared with healthy controls (P < 0.001). Serum Sclerostin and Dickkopf-1 levels were significantly correlated with serum fluoride in all studied subjects (n = 186). Low Sclerostin and Dickkopf-1 levels were associated with a significantly increased risk of fluorine bone injury. In conclusion, serum Sclerostin and Dickkopf-1 might be used as important markers of bone metabolism change and potential therapeutic targets to treat fluorine bone injury. (c) 2013 Elsevier B.V. All rights reserved.

引用

页码：402 / 407

页数：6

共 25 条

[1] Identification of a 52 kb deletion downstream of the SOST gene in patients with van Buchem disease [J].