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3 Department of Physiology, Pediatrics, and 2 Division of Gastroentrology, Department of Medicine, and 1 Eudowood Division of Respiratory Sciences, The Johns Hopkins School of Medicine, The Johns Hopkins University, Baltimore, Maryland 21205
Mutations in the chloride channel, ClC-5, have been described in
several inherited diseases that result in the formation of kidney
stones. To determine whether ClC-5 is also involved in calcium
homeostasis, we investigated whether ClC-5 mRNA and protein expression
are modulated in rats deficient in 1
,25(OH)2 vitamin
D3 with and without thyroparathyroidectomy. Parathyroid hormone (PTH) was replaced in some animals. Vitamin D-deficient, thyroparathyrodectomized rats had lower serum and higher urinary calcium concentrations compared with control animals as well as lower
serum PTH and calcitonin concentrations. ClC-5 mRNA and protein levels
in the cortex decrease in vitamin D-deficient, thyroparathyroidectomized rats compared with both control and vitamin
D-deficient animals. ClC-5 mRNA and protein expression increase near to
control levels in vitamin D-deficient, thyroparathyroidectomized rats
injected with PTH. No significant changes in ClC-5 mRNA and protein
expression in the medulla were detected in any experimental group. Our
results suggest that PTH modulates the expression of ClC-5 in the
kidney cortex and that neither 1,25(OH)2 vitamin D3 nor PTH regulates ClC-5 expression in the medulla. The
pattern of expression of ClC-5 varies with urinary calcium. Animals
with higher urinary calcium concentrations have lower levels of ClC-5 mRNA and protein expression, suggesting that the ClC-5 chloride channel
plays a role in calcium reabsorption.
chloride channels; kidney stones; nephrolithiasis
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