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

Abstract：

: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-dihydroxyvitamin 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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Shimada T,Urakawa I,Yamazaki Y,Hasegawa H,Hino R,Yoneya T,Takeuchi Y,Fujita T,Fukumoto S,Yamashita T

doi

10.1016/j.bbrc.2003.12.102

subject

Has Abstract

pub_date

2004-02-06 00:00:00

pages

409-14

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006291X03026378

journal_volume

314

pub_type

杂志文章

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