ClC-5 regulates dentin development through TGF-β1 pathway

被引：18

作者：

Duan, Xiaohong ^{[1
]}

Mao, Yong ^{[2
]}

Yang, Ting ^{[1
]}

Wen, Xuan ^{[1
]}

Wang, Huan ^{[3
]}

Hou, Jin ^{[1
]}

Xue, Yang ^{[4
]}

Zhang, Rong ^{[5
]}

机构：

[1] Fourth Mil Med Univ, Sch Stomatol, Dept Oral Biol, Xian 710032, Shaanxi, Peoples R China

[2] Fourth Mil Med Univ, Sch Stomatol, Dept Prosthodont, Xian 710032, Shaanxi, Peoples R China

[3] Fourth Mil Med Univ, Sch Stomatol, Dept Orthodont, Xian 710032, Shaanxi, Peoples R China

[4] Fourth Mil Med Univ, Sch Stomatol, Dept Oral Surg, Xian 710032, Shaanxi, Peoples R China

[5] Fourth Mil Med Univ, Sch Stomatol, Dept Endodont, Xian 710032, Shaanxi, Peoples R China

来源：

ARCHIVES OF ORAL BIOLOGY | 2009年 / 54卷 / 12期

基金：

中国国家自然科学基金;

关键词：

ClC-5; Dentin; Odontoblast; TGF-beta; 1; Chloride channel; CHLORIDE CHANNELS; DENTINOGENESIS IMPERFECTA; TISSUE DISTRIBUTION; MOUSE MODEL; EXPRESSION; CELLS; LOCALIZATION; DISEASES; CLONING; KIDNEY;

D O I：

10.1016/j.archoralbio.2009.09.008

中图分类号：

R78 [口腔科学];

学科分类号：

1003 ;

摘要：

ClC-5 is one of the voltage-dependent chloride channel (ClC) family members. Mutations involving CLCN5 cause an X-linked nephropathy associated with Dent's disease. Some Clcn5 gene knockout (ClC-5 KO) mice have abnormal growth of the teeth; however, the expression and function of ClC-5 during tooth development is still unknown. Herein we report abnormal dentin structure, decreased DSPP and increased TGF-beta 1 protein level in ClC-5 KO teeth. In odontoblast-like MDPC-23 cells, the mRNA levels of Tgfb1, Dspp and Dmp-1 were upregulated with Clcn5 RNAi after 48 h treatment; whilst there was no change in those of TGF-beta receptor Tgfbr1 and Tgfbr2. We suggest that the dentin changes in ClC-5 KO mice might be a result of increasing TGF-beta 1, and the interplay between ClC-5 and TGF-beta 1 needs further identified. (C) 2009 Elsevier Ltd. All rights reserved.

引用

页码：1118 / 1124

页数：7

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