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Published ahead of print on July 23, 2009
J Am Soc Nephrol 20: 2009-2017, 2009
© 2009 American Society of Nephrology
doi: 10.1681/ASN.2008121258
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BASIC RESEARCH

Indirect Regulation of PTH by Estrogens May Require FGF23

Natalia Carrillo-López, Pablo Román-García, Ana Rodríguez-Rebollar, José Luis Fernández-Martín, Manuel Naves-Díaz and Jorge B. Cannata-Andía

Bone and Mineral Research Unit, Hospital Universitario Central de Asturias, Instituto Reina Sofía de Investigación, REDinREN del ISCIII, Universidad de Oviedo, Oviedo, Asturias, Spain

Correspondence: Jorge B. Cannata-Andía, Bone and Mineral Research Unit, Instituto Reina Sofía de Investigación, Hospital Universitario Central de Asturias, C/ Julián Clavería s/n, 33006 Oviedo, Asturias, Spain. Phone: 34-985-106-137; Fax: 34-985-106-142; E-mail: metoseo{at}hca.es

Received for publication December 12, 2008. Accepted for publication May 13, 2009.

The mechanisms by which estrogens modulate PTH are controversial, including whether or not estrogen receptors (ERs) are present in the parathyroid glands. To explore these mechanisms, we combined a rat model of CKD with ovariectomy and exogenous administration of estrogens. We found that estrogen treatment significantly decreased PTH mRNA and serum levels. We did not observe ER{alpha} or ERβ mRNA or protein in the parathyroids, suggesting an indirect action of estrogens on PTH regulation. Estrogen treatment significantly decreased serum 1,25(OH)2 vitamin D3 and phosphorus levels. In addition, estrogens significantly increased fibroblast growth factor 23 (FGF23) mRNA and serum levels. In vitro, estrogens led to transcriptional and translational upregulation of FGF23 in osteoblast-like cells in a time- and concentration-dependent manner. These results suggest that estrogens regulate PTH indirectly, possibly through FGF23.






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Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673