Ion Channels – Membrane Transport – Integrative Physiology
Kidney International (2004) 66, 1082–1089; doi:10.1111/j.1523-1755.2004.00858.x
Effects of vitamin D compounds on renal and intestinal Ca2+ transport proteins in 25-hydroxyvitamin D3-1
-hydroxylase knockout mice1
JOOST G J HOENDEROP, ANNEMIETE W C M VAN DER KEMP, COLLEEN M URBEN, STEPHEN A STRUGNELL and RENÉ J M BINDELS
Department of Physiology, Nijmegen Centre for Molecular Life Sciences, University Medical Centre Nijmegen, The Netherlands; and Bone Care International, Middleton, Wisconsin
Correspondence: René J.M. Bindels, 160 Physiology University Medical Centre Nijmegen, P.O. Box 9101, NL-6500 HB Nijmegen, The Netherlands. E-mail:r.bindels@ncmls.kun.nl
1See Editorial by Goodman, p. 1286.
Received 16 January 2004; Revised 24 March 2004; Accepted 16 April 2004.
Abstract
Effects of vitamin D compounds on renal and intestinal Ca2+ transport proteins in 25-hydroxyvitamin D3-1
-hydroxylase knockout mice.
Background
Vitamin D compounds are used clinically to control secondary hyperparathyroidism (SHPT) due to renal failure. Newer vitamin D compounds retain the suppressive action of 1,25(OH)2D3 on the parathyroid glands and may have less Ca2+-mobilizing activity, offering potentially safer therapies.
Methods
This study investigated the effect of a single dose of compound (1,25(OH)2D3, 1,24(OH)2D2, or 1
(OH)D2) on renal and intestinal Ca2+ transport proteins, including TRPV5 and TRPV6, and serum Ca2+, in a novel SHPT model, the 25-OH-D3-1
-hydroxylase knockout mouse, which lacks endogenous 1,25(OH)2D3 and is severely hypocalcemic. Animals were injected intraperitoneally with compound (100 ng/mouse).
Results
Serum levels of 1,25(OH)2D3 and 1,24(OH)2D2 peaked at four hours post-injection (pi), then declined rapidly. 1,25(OH)2D2 generated from 1
(OH)D2 peaked at 12 hours pi and then remained stable. Serum Ca2+ was increased to near-normal within four hours by 1,25(OH)2D3 and 1,24(OH)2D2, and within 12 hours by 1
(OH)D2. 1,25(OH)2D3 and 1,24(OH)2D2 up-regulated duodenal TRPV5 and TRPV6 mRNA to a similar degree within four hours; mRNA levels decreased by 12 hours after 1,24(OH)2D2 treatment, and by 24 hours after 1,25(OH)2D3 treatment. 1,25(OH)2D3 increased kidney levels of TRPV5, calbindin-D28K, and calbindin-D9K mRNA within four hours; 1,24(OH)2D2 did not change kidney TRPV5 levels and modestly increased calbindin D9K by 48 hours. 1
(OH)D2 produced later-onset effects, increasing duodenal TRPV6 and calbindin-D9K mRNA levels by 12 hours and TRPV5 by 48 hours.
Conclusion
In kidney, 1
(OH)D2 increased TRPV5, calbindin-D28K, and calbindin-D9K mRNA levels by 12 hours. This study indicates that Ca2+ transport proteins, including TRPV5 and TRPV6, are differentially up-regulated by vitamin D compounds.
Keywords:
ECaC1, CaT1, TRPV5, TRPV6, calcium reabsorption, vitamin D, secondary hyperparathyroidism
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