The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
PTH increases FGF23 gene expression and mediates the high-FGF23 levels of experimental kidney failure: a bone parathyroid feedback loop
Abstract
Parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) target the kidney to cause a phosphaturia. FGF23 also acts on the parathyroid to decrease PTH expression, but in chronic kidney disease (CKD) there are high-serum PTH and FGF23 levels and resistance of the parathyroid to FGF23. We now report that PTH acts on bone to increase FGF23 expression and characterize the signal transduction pathway whereby PTH increases FGF23 expression. Remarkably, we show that PTH is necessary for the high-FGF23 levels of early kidney failure due to an adenine high-phosphorus diet. Parathyroidectomy before the diet totally prevented the fivefold increase in FGF23 levels in kidney failure rats. Moreover, parathyroidectomy of early kidney failure rats corrected their high-FGF23 levels. Therefore, in early kidney failure, the high-FGF23 levels are dependent on the high-PTH levels. PTH infusion for 3 days to mice with normal renal function increased serum FGF23 and calvaria FGF23 mRNA levels. To demonstrate a direct effect of PTH on FGF23, we added PTH to rat osteoblast-like UMR106 cells. PTH increased FGF23 mRNA levels (4-fold) and this effect was mimicked by a PKA activator, forskolin. PTH also decreased SOST mRNA levels (3-fold). SOST codes for sclerostin, a Wnt pathway inhibitor, which is a PTH receptor (PTH1R) target. The effect of PTH was prevented by added sclerostin. Therefore, PTH increases FGF23 expression which involves the PKA and Wnt pathways. The effect of PTH on FGF23 completes a bone-parathyroid endocrine feedback loop. Importantly, secondary hyperparathyroidism is essential for the high-FGF23 levels in early CKD.
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Cites
FGF-23 Is a Potent Regulator of Vitamin D Metabolism and Phosphate Homeostasis
Shimada, T., Hasegawa, H., Yamazaki, Y., Muto, T., Hino, R., Takeuchi, Y., Fujita, T., Nakahara, K., Fukumoto, S., & Yamashita, T. (2004) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.0301264 · Cited by 1,883
Klotho converts canonical FGF receptor into a specific receptor for FGF23
Urakawa, I., Yamazaki, Y., Shimada, T., Iijima, K., Hasegawa, H., Okawa, K., Fujita, T., Fukumoto, S., & Yamashita, T. (2006) · Nature · doi:10.1038/nature05315 · Cited by 1,850
Fibroblast Growth Factor 23 and Mortality among Patients Undergoing Hemodialysis
Gutiérrez, O. M., Mannstadt, M., Isakova, T., Rauh-Hain, J. A., Tamez, H., Shah, A., Smith, K., Lee, H., Thadhani, R., Jüppner, H., et al. (2008) · New England Journal of Medicine · doi:10.1056/nejmoa0706130 · Cited by 1,727
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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Regulation of Fibroblast Growth Factor-23 Signaling by Klotho
Kurosu, H., Ogawa, Y., Miyoshi, M., Yamamoto, M., Nandi, A., Rosenblatt, K. P., Baum, M. G., Schiavi, S., Hu, M.-C., Moe, O. W., et al. (2006) · Journal of Biological Chemistry · doi:10.1074/jbc.c500457200 · Cited by 1,366
The parathyroid is a target organ for FGF23 in rats
Ben-Dov, I. Z., Galitzer, H., Lavi-Moshayoff, V., Goetz, R., Kuro-o, M., Mohammadi, M., Sirkis, R., Naveh-Many, T., & Silver, J. (2007) · Journal of Clinical Investigation · doi:10.1172/jci32409 · Cited by 951
Self-citationMolecular and cellular mechanisms of the anabolic effect of intermittent PTH
Jilka, R. L. (2007) · Bone · doi:10.1016/j.bone.2007.03.017 · Cited by 720
Fibroblast Growth Factor 23 Is a Counter-Regulatory Phosphaturic Hormone for Vitamin D
Liu, S., Tang, W., Zhou, J., Stubbs, J. R., Luo, Q., Pi, M., & Quarles, L. D. (2006) · Journal of the American Society of Nephrology · doi:10.1681/asn.2005111185 · Cited by 642
Bellido, T., Ali, A. A., Gubrij, I., Plotkin, L. I., Fu, Q., O’Brien, C. A., Manolagas, S. C., & Jilka, R. L. (2005) · Endocrinology · doi:10.1210/en.2005-0239 · Cited by 641
Cited by
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
The Klotho proteins in health and disease
Kuro-o, M. (2019) · Nature Reviews Nephrology · doi:10.1038/s41581-018-0078-3 · Cited by 707
Regulation and Function of the FGF23/Klotho Endocrine Pathways
Martin, A., David, V., & Quarles, L. D. (2012) · Physiological Reviews · doi:10.1152/physrev.00002.2011 · Cited by 594
Hu, M. C., Shiizaki, K., Kuro-o, M., & Moe, O. W. (2013) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183727 · Cited by 587
Therapeutic potential of the endocrine fibroblast growth factors FGF19, FGF21 and FGF23
Degirolamo, C., Sabbà, C., & Moschetta, A. (2016) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2015.9 · Cited by 424
Metadata
- Authors
- Lavi-Moshayoff, V., Wasserman, G., Meir, T., Silver, J., & Naveh-Many, T.
- Venue
- American Journal of Physiology-Renal Physiology
- Publisher
- American Physiological Society
- Published
- 2010-10
- Volume
- 299
- Issue
- 4
- Pages
- F882-F889
- ISSN
- 1522-1466 (ISSN-L)
- 1931-857X
- OpenAlex
- W2041242683
- Cited by
- 441
- References
- 47
- FWCI
- 24.72
- Type
- journal article
- Language
- en
- Open access
- closed
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- Lavi-Moshayoff, V., Wasserman, G., Meir, T., Silver, J., & Naveh-Many, T. (2010). PTH increases FGF23 gene expression and mediates the high-FGF23 levels of experimental kidney failure: a bone parathyroid feedback loop. American Journal of Physiology-Renal Physiology. https://doi.org/10.1152/ajprenal.00360.2010
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