FGF-23 inhibits renal tubular phosphate transport and is a PHEX substrate.

Abstract:

:Oncogenic osteomalacia (OOM), X-linked hypophosphatemia (XLH), and autosomal dominant hypophosphatemic rickets (ADHR) are phenotypically similar disorders characterized by hypophosphatemia, decreased renal phosphate reabsorption, normal or low serum calcitriol concentrations, normal serum concentrations of calcium and parathyroid hormone, and defective skeletal mineralization. XLH results from mutations in the PHEX gene, encoding a membrane-bound endopeptidase, whereas ADHR is associated with mutations of the gene encoding FGF-23. Recent evidence that FGF-23 is expressed in mesenchymal tumors associated with OOM suggests that FGF-23 is responsible for the phosphaturic activity previously termed "phosphatonin." Here we show that both wild-type FGF-23 and the ADHR mutant, FGF-23(R179Q), inhibit phosphate uptake in renal epithelial cells. We further show that the endopeptidase, PHEX, degrades native FGF-23 but not the mutant form. Our results suggest that FGF-23 is involved in the pathogenesis of these three hypophosphatemic disorders and directly link PHEX and FGF-23 within the same biochemical pathway.

authors

Bowe AE,Finnegan R,Jan de Beur SM,Cho J,Levine MA,Kumar R,Schiavi SC

doi

10.1006/bbrc.2001.5084

subject

Has Abstract

pub_date

2001-06-22 00:00:00

pages

977-81

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(01)95084-3

journal_volume

284

pub_type

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