The DOI matches its Crossref record; 80 of the 80 references it cites were found in a registry or an index.
FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1
Open accessAbstract
Fibroblast growth factor-23 (FGF23) is a phosphaturic hormone that contributes to several hypophosphatemic disorders by reducing the expression of the type II sodium-phosphate cotransporters (NaPi-2a and NaPi-2c) in the kidney proximal tubule and by reducing serum 1,25-dihydroxyvitamin D 3[1,25(OH)2 D 3] levels. The FGF receptor(s) mediating the hypophosphatemic action of FGF23 in vivo have remained elusive. In this study, we show that proximal tubules express FGFR1, −3, and −4 but not FGFR2 mRNA. To determine which of these three FGFRs mediates FGF23's hypophosphatemic actions, we characterized phosphate homeostasis in FGFR3−/−and FGFR4−/−null mice, and in conditional FGFR1−/−mice, with targeted deletion of FGFR1 expression in the metanephric mesenchyme. Basal serum phosphorus levels and renal cortical brush-border membrane (BBM) NaPi-2a and NaPi-2c expression were comparable between FGFR1−/−, FGFR3−/−, and FGFR4−/−mice and their wild-type counterparts. Administration of FGF23 to FGFR3−/−mice induced hypophosphatemia in these mice (8.0 ± 0.4 vs. 5.4 ± 0.3 mg/dl; p ≤ 0.001) and a decrease in renal BBM NaPi-2a and NaPi-2c protein expression. Similarly, in FGFR4−/−mice, administration of FGF23 caused a small but significant decrease in serum phosphorus levels (8.7 ± 0.3 vs. 7.6 ± 0.4 mg/dl; p ≤ 0.001) and in renal BBM NaPi-2a and NaPi-2c protein abundance. In contrast, injection of FGF23 into FGFR1−/−mice had no effects on serum phosphorus levels (5.6 ± 0.3 vs. 5.2 ± 0.5 mg/dl) or BBM NaPi-2a and NaPi-2c expression. These data show that FGFR1 is the predominant receptor for the hypophosphatemic action of FGF23 in vivo, with FGFR4 likely playing a minor role.
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Cites
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Klotho converts canonical FGF receptor into a specific receptor for FGF23
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Cited by
The Osteocyte: An Endocrine Cell … and More
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FGF/FGFR signaling in health and disease
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Regulation of Phosphate Homeostasis by PTH, Vitamin D, and FGF23
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Regulation and Function of the FGF23/Klotho Endocrine Pathways
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The FGF23–Klotho axis: endocrine regulation of phosphate homeostasis
Razzaque, M. S. (2009) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2009.196 · Cited by 448
Metadata
- Authors
- Gattineni, J., Bates, C., Twombley, K., Dwarakanath, V., Robinson, M. L., Goetz, R., Mohammadi, M., & Baum, M.
- Venue
- American Journal of Physiology-Renal Physiology
- Publisher
- American Physiological Society
- Published
- 2009-08
- Volume
- 297
- Issue
- 2
- Pages
- F282-F291
- ISSN
- 1522-1466 (ISSN-L)
- 1931-857X
- OpenAlex
- W2139989191
- Cited by
- 438
- References
- 80
- FWCI
- 15.46
- Type
- journal article
- Language
- en
- Open access
- green
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- Gattineni, J., Bates, C., Twombley, K., Dwarakanath, V., Robinson, M. L., Goetz, R., Mohammadi, M., & Baum, M. (2009). FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1. American Journal of Physiology-Renal Physiology. https://doi.org/10.1152/ajprenal.90742.2008
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