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Influence of the in Vivo Calcium Status on Cellular Calcium Homeostasis and the Level of the Calcium-Binding Protein Calreticulin in Rat Hepatocytes¹

Centre de Recherche, Hôpital Saint-Luc, Centre Hospitalier de l’Université de Montréal (G.M., J.-L.P., C.D., M.G.-B.), and Départements de Nutrition (G.M., M.G.-B.) and Pharmacologie (M.G.-B.), Faculté de Médecine, Université de Montréal, Montréal, Québec, Canada H2X 1P1

Address all correspondence and requests for reprints to: Dr. Marielle Gascon-Barré, Centre de Recherche, Hôpital Saint-Luc, Centre Hospitalier de l’Université de Montréal, 264 René-Lévesque boulevard East, Montréal, Québec, Canada H2X 1P1. E-mail: marielle.gascon.barre{at}umontreal.ca

Little attention has been given to the consequences of the in vivo calcium status on intracellular calcium homeostasis despite several pathological states induced by perturbations of the in vivo calcium balance. The aim of these studies was to probe the influence of an in vivo calcium deficiency on the resting cytoplasmic Ca²⁺ concentration and the inositol-1,4,5-trisphosphate-sensitive Ca²⁺ pools. Studies were conducted in hepatocytes (a cell type well characterized for its cellular Ca²⁺ response) isolated from normal and calcium-deficient rats secondary to vitamin D depletion. Both resting cytoplasmic Ca²⁺ concentration and Ca²⁺ mobilization from inositol-1,4,5-trisphosphate -sensitive cellular pools were significantly lowered by calcium depletion. In addition, Ca deficiency was shown to significantly reduce calreticulin messenger RNA and protein levels but calcium entry through store-operated calcium channels remained unaffected, indicating that the Ca²⁺ entry mechanisms are still fully operational in calcium deficiency. The effects of calcium deficiency on cellular calcium homeostasis were reversible by repletion with oral calcium feeding alone or by the administration of the calcium-regulating hormone 1,25-dihydroxyvitamin D₃, further strengthening the tight link between extra- and intracellular calcium. These data, therefore, challenge the currently prevailing hypothesis that extracellular Ca²⁺ has no significant impact on cellular Ca²⁺ by demonstrating that despite the large Ca²⁺ gradient between extra- and intracellular Ca²⁺ concentrations, calcium deficiency in vivo significantly alters the hormone-sensitive cellular calcium homeostasis.

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