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

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 m...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2004-02, Vol.314 (2), p.409-414
Main Authors: Shimada, Takashi, Urakawa, Itaru, Yamazaki, Yuji, Hasegawa, Hisashi, Hino, Rieko, Yoneya, Takashi, Takeuchi, Yasuhiro, Fujita, Toshiro, Fukumoto, Seiji, Yamashita, Takeyoshi
Format: Article
Language:English
Subjects:
1,25-Dihydroxyvitamin D
Animals
Animals, Newborn
Bone and Bones - diagnostic imaging
FGF-23
Fibroblast Growth Factors - genetics
Fibroblast Growth Factors - physiology
Humans
Hypophosphatemic rickets
Immunohistochemistry
Kidney Tubules - metabolism
Mice
Mice, Transgenic
Plasmids - metabolism
Radiography
Reverse Transcriptase Polymerase Chain Reaction
Rickets - genetics
Sodium phosphate cotransporter type IIa
Sodium-Phosphate Cotransporter Proteins
Sodium-Phosphate Cotransporter Proteins, Type IIa
Symporters - biosynthesis
Symporters - genetics
Time Factors
Tissue Distribution
Transgenes
Vitamin D - analogs & derivatives
Vitamin D - blood
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Summary: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.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2003.12.102