The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index.
Transgenic Mice Expressing Fibroblast Growth Factor 23 under the Control of the α1(I) Collagen Promoter Exhibit Growth Retardation, Osteomalacia, and Disturbed Phosphate Homeostasis
Abstract
Mutations in the fibroblast growth factor 23 gene, FGF23, cause autosomal dominant hypophosphatemic rickets (ADHR). The gene product, FGF-23, is produced by tumors from patients with oncogenic osteomalacia (OOM), circulates at increased levels in most patients with X-linked hypophosphatemia (XLH) and is phosphaturic when injected into rats or mice, suggesting involvement in the regulation of phosphate (Pi) homeostasis. To better define the precise role of FGF-23 in maintaining Pi balance and bone mineralization, we generated transgenic mice that express wild-type human FGF-23, under the control of the alpha1(I) collagen promoter, in cells of the osteoblastic lineage. At 8 wk of age, transgenic mice were smaller (body weight = 17.5 +/- 0.57 vs. 24.3 +/- 0.37 g), exhibited decreased serum Pi concentrations (1.91 +/- 0.27 vs. 2.75 +/- 0.22 mmol/liter) and increased urinary Pi excretion when compared with wild-type littermates. The serum concentrations of human FGF-23 (undetectable in wild-type mice) was markedly elevated in transgenic mice (>7800 reference units/ml). Serum PTH levels were increased in transgenic mice (231 +/- 62 vs. 139 +/- 44 pg/ml), whereas differences in calcium and 1,25-dihydroxyvitamin D were not apparent. Expression of Npt2a, the major renal Na(+)/Pi cotransporter, as well as Npt1 and Npt2c mRNAs, was significantly decreased in the kidneys of transgenic mice. Histology of tibiae displayed a disorganized and widened growth plate and peripheral quantitative computerized tomography analysis revealed reduced bone mineral density in transgenic mice. The data indicate that FGF-23 induces phenotypic changes in mice resembling those of patients with ADHR, OOM, and XLH and that FGF-23 is an important determinant of Pi homeostasis and bone mineralization.
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Autosomal dominant hypophosphataemic rickets is associated with mutations in FGF23
White, K. E., Evans, W. E., O'Riordan, J. L. H., Speer, M. C., Econs, M. J., Lorenz-Depiereux, B., Grabowski, M., Meitinger, T., & Strom, T. M. (2000) · Nature Genetics · doi:10.1038/81664 · Cited by 1,528
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Fibroblast Growth Factor 23 in Oncogenic Osteomalacia and X-Linked Hypophosphatemia
Jonsson, K. B., Zahradnik, R., Larsson, T., White, K. E., Sugimoto, T., Imanishi, Y., Yamamoto, T., Hampson, G., Koshiyama, H., Ljunggren, Ö., et al. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa020881 · Cited by 914
Self-citationLarsson, T., Nisbeth, U. L. F., Ljunggren, Ö., Jüppner, H., & Jonsson, K. B. (2003) · Kidney International · doi:10.1046/j.1523-1755.2003.00328.x · Cited by 689
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FGF-23 in fibrous dysplasia of bone and its relationship to renal phosphate wasting
Riminucci, M., Collins, M. T., Fedarko, N. S., Cherman, N., Corsi, A., White, K. E., Waguespack, S., Gupta, A., Hannon, T., Econs, M. J., et al. (2003) · Journal of Clinical Investigation · doi:10.1172/jci18399 · Cited by 657
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Self-citationRegulation of Fibroblastic Growth Factor 23 Expression but Not Degradation by PHEX
Liu, S., Guo, R., Simpson, L. G., Xiao, Z.-S., Burnham, C. E., & Quarles, L. D. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m304544200 · Cited by 508
Cited by
The FGF family: biology, pathophysiology and therapy
Beenken, A., & Mohammadi, M. (2009) · Nature Reviews Drug Discovery · doi:10.1038/nrd2792 · Cited by 1,945
Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice
Bouillon, R., Carmeliet, G., Verlinden, L., van Etten, E., Verstuyf, A., Luderer, H. F., Lieben, L., Mathieu, C., & Demay, M. (2008) · Endocrine Reviews · doi:10.1210/er.2008-0004 · Cited by 1,783
Receptor Specificity of the Fibroblast Growth Factor Family
Zhang, X., Ibrahimi, O. A., Olsen, S. K., Umemori, H., Mohammadi, M., & Ornitz, D. M. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.m601252200 · Cited by 1,164
The Osteocyte: An Endocrine Cell … and More
Dallas, S. L., Prideaux, M., & Bonewald, L. F. (2013) · Endocrine Reviews · doi:10.1210/er.2012-1026 · Cited by 1,042
FGF/FGFR signaling in health and disease
Xie, Y., Su, N., Yang, J., Tan, Q., Huang, S., Jin, M., Ni, Z., Zhang, B., Zhang, D., Luo, F., et al. (2020) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-020-00222-7 · Cited by 904
Metadata
- Authors
- Larsson, T., Marsell, R., Schipani, E., Ohlsson, C., Ljunggren, Ö., Tenenhouse, H. S., Jüppner, H., & Jonsson, K. B.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2004-07
- Volume
- 145
- Issue
- 7
- Pages
- 3087-3094
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2128059069
- Cited by
- 499
- References
- 40
- FWCI
- 18.99
- Type
- journal article
- Language
- en
- Open access
- closed
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- Larsson, T., Marsell, R., Schipani, E., Ohlsson, C., Ljunggren, Ö., Tenenhouse, H. S., Jüppner, H., & Jonsson, K. B. (2004). Transgenic Mice Expressing Fibroblast Growth Factor 23 under the Control of the α1(I) Collagen Promoter Exhibit Growth Retardation, Osteomalacia, and Disturbed Phosphate Homeostasis. Endocrinology. https://doi.org/10.1210/en.2003-1768
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