FGF-23 transgenic mice demonstrate hypophosphatemic rickets with reduced expression of sodium phosphate cotransporter type IIa

被引：338

作者：

Shimada, T

Urakawa, I

Yamazaki, Y

Hasegawa, H

Hino, R

Yoneya, T

Takeuchi, Y

Fujita, T

Fukumoto, S

Yamashita, T

机构：

[1] Kirin Brewery Co Ltd, Pharmaceut Res Labs, Gunma 3701295, Japan

[2] Univ Tokyo, Sch Med, Dept Med, Div Endocrinol,Bunkyo Ku, Tokyo 1138655, Japan

[3] Tokyo Univ Hosp, Dept Lab Med, Bunkyo Ku, Tokyo 1138655, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2004年 / 314卷 / 02期

关键词：

FGF-23; hypophosphatemic rickets; 1,25-dihydroxyvitamin D; sodium phosphate cotransporter type IIa;

D O I：

10.1016/j.bbrc.2003.12.102

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Fibroblast growth factor (FGF)-23 was identified as a causative factor of tumor-induced osteomalacia and also as a responsible gene for autosomal dominant hypophosphatemic rickets. To clarify the pathophysiological roles of FGF-23 in these diseases, we generated its transgenic mice. The transgenic mice expressing human FGF-23 reproduced the common clinical features of these diseases such as hypophosphatemia probably due to increased renal phosphate wasting, inappropriately low serum 1,25-di-hydroxyvitamin D level, and rachitic bone. The renal phosphate wasting in the transgenic mice was accompanied by the reduced expression of sodium phosphate cotransporter type IIa in renal proximal tubules. These results reinforce the notion that the excessive action of FGF-23 plays a causative role in the development of several hypophosphatemic rickets/osteomalacia. (C) 2003 Elsevier Inc. All rights reserved.

引用

页码：409 / 414

页数：6