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-hydroxylase knockout mice
Department of Cell Physiology, University Medical Centre Nijmegen, 6500 HB Nijmegen, Netherlands; and
* Genetics Unit, Shriners Hospital for Children, Montreal, Quebec, Canada
1Correspondence: 160 Cell Physiology, Nijmegen Centre for Molecular Life Sciences, University Medical Centre Nijmegen, P.O. Box 9101, NL-6500 HB Nijmegen, Netherlands. Express mail: M850 Room 07.048, Centrale Ontvangst Goederen, Geert Grooteplein Zuid 30, NL-6525 GA Nijmegen, Netherlands. E-mail: r.bindels{at}ncmls.kun.nl
Pseudovitamin D-deficiency rickets (PDDR) is an autosomal disease characterized by hyperparathyroidism, rickets, and undetectable levels of 1,25-dihydroxyvitaminD3 (1,25(OH)2D3). Mice in which the 25-hydroxyvitamin D3-1
-hydroxylase (1-OHase) gene was inactivated presented the same clinical phenotype as patients with PDDR and were used to study renal expression of the epithelial Ca2+ channel (ECaC1), the calbindins, Na+/Ca2+ exchanger (NCX1), and Ca2+-ATPase (PMCA1b). Serum Ca2+ (1.20±0.05 mM) and mRNA/protein expression of ECaC1 (41±3%), calbindin-D28K (31±2%), calbindin-D9K (58±7%), NCX1 (10±2%), PMCA1b (96±4%) were decreased in 1-OHase-/- mice compared with 1-OHase+/- littermates. Feeding these mice a Ca2+-enriched diet normalized serum Ca2+ levels and expression of Ca2+ proteins except for calbindin-D9K expression. 1,25(OH)2D3 repletion resulted in increased expression of Ca2+ transport proteins and normalization of serum Ca2+ levels. Localization of Ca2+ transport proteins was clearly polarized in which ECaC1 was localized along the apical membrane, calbindin-D28K in the cytoplasm, and calbindin-D9K along the apical and basolateral membranes, resulting in a comprehensive mechanism facilitating renal transcellular Ca2+ transport. This study demonstrated that high dietary Ca2+ intake is an important regulator of the renal Ca2+ transport proteins in 1,25(OH)2D3-deficient status and thus contributes to the normalization of blood Ca2+ levels.—Hoenderop, J. G. J., Dardenne, O., van Abel, M., van der Kemp, A. W. C. M., van Os, C. H., St.-Arnaud, R., Bindels, R. J. M. Modulation of renal Ca2+ transport protein genes by dietary Ca2+ and 1,25-dihydroxyvitamin D3 in 25-hydroxyvitamin D3-1-hydroxylase knockout mice.
Key Words: ECaC • CaT1 • vitamin D • calcium reabsorption
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