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J Am Soc Nephrol 13:2102-2109, 2002
© 2002 American Society of Nephrology

1,25-Dihydroxyvitamin D3-Independent Stimulatory Effect of Estrogen on the Expression of ECaC1 in the Kidney

Monique van Abel*, Joost G. J. Hoenderop*, Olivier Dardenne{dagger}, René St. Arnaud{dagger}, Carel H. van Os*, Hans J. P. T. M. van Leeuwen{ddagger} and René J. M. Bindels*

*Department of Cell Physiology, Nijmegen Center for Molecular Life Sciences, University Medical Center Nijmegen, Nijmegen, The Netherlands; {dagger}Genetics Unit, Shriners Hospital for Children, Montreal, Quebec, Canada; and {ddagger}Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands.

Correspondence to Dr. René J. M. Bindels, 160 Cell Physiology, University Medical Center Nijmegen, P.O. Box 9101, NL-6500 HB Nijmegen, The Netherlands. Phone: +31-24-3614211; Fax: +31-24-3616413; E-mail: r.bindels{at}ncmls.kun.nl

ABSTRACT. Estrogen deficiency results in a negative Ca2+ balance and bone loss in postmenopausal women. In addition to bone, the intestine and kidney are potential sites for estrogen action and are involved in Ca2+ handling and regulation. The epithelial Ca2+ channel ECaC1 (or TRPV5) is the entry channel involved in active Ca2+ transport. Ca2+ entry is followed by cytosolic diffusion, facilitated by calbindin-D28K and/or calbindin-D9k, and active extrusion across the basolateral membrane by the Na+/Ca2+-exchanger (NCX1) and plasma membrane Ca2+-ATPase (PMCA1b). In this transcellular Ca2+ transport, ECaC1 probably represents the final regulatory target for hormonal control. The aim of this study was to determine whether 17{beta}-estradiol (17{beta}-E2) is involved in Ca2+ reabsorption via regulation of the expression of ECaC1. The ovariectomized rat model was used to investigate the regulation of ECaC1, at the mRNA and protein levels, by 17{beta}-E2 replacement therapy. Using real-time quantitative PCR and immunohistochemical analyses, this study demonstrated that 17{beta}-E2 treatment at pharmacologic doses increased renal mRNA levels of ECaC1, calbindin-D28K, NCX1, and PMCA1b and increased the protein abundance of ECaC1. Furthermore, the involvement of 1,25-dihydroxyvitamin D3 in the effects of 17{beta}-E2 was examined in 25-hydroxyvitamin D3-1{alpha}-hydroxylase-knockout mice. Renal mRNA expression of calbindin-D9K, calbindin-D28K, NCX1, and PMCA1b was not significantly altered after 17{beta}-E2 treatment. In contrast, ECaC1 mRNA and protein levels were both significantly upregulated. Moreover, 17{beta}-E2 treatment partially restored serum Ca2+ levels, from 1.63 ± 0.06 to 2.03 ± 0.12 mM. In conclusion, this study suggests that 17{beta}-E2 is positively involved in renal Ca2+ reabsorption via the upregulation of ECaC1, an effect independent of 1,25-dihydroxyvitamin D3.




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