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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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  K. Kawaai, C. Hisatsune, Y. Kuroda, A. Mizutani, T. Tashiro, and K. Mikoshiba 80K-H Interacts with Inositol 1,4,5-Trisphosphate (IP3) Receptors and Regulates IP3-induced Calcium Release Activity J. Biol. Chem., January 2, 2009; 284(1): 372 - 380. [Abstract] [Full Text] [PDF]
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T.-M. Nguyen, M. Lieberherr, J. Fritsch, H. Guillozo, M. L. Alvarez, Z. Fitouri, F. Jehan, and M. Garabedian The Rapid Effects of 1,25-Dihydroxyvitamin D3 Require the Vitamin D Receptor and Influence 24-Hydroxylase Activity: STUDIES IN HUMAN SKIN FIBROBLASTS BEARING VITAMIN D RECEPTOR MUTATIONS J. Biol. Chem., February 27, 2004; 279(9): 7591 - 7597. [Abstract] [Full Text] [PDF]
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 S. J. Provencher and M. Gascon-Barre Effect of Cyclosporine A on Hepatic Compensatory Growth: Role of Calcium Status J. Pharmacol. Exp. Ther., October 1, 2002; 303(1): 58 - 65. [Abstract] [Full Text] [PDF]
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 A. Elimadi and P. S. Haddad Cold preservation-warm reoxygenation increases hepatocyte steady-state Ca2+ and response to Ca2+-mobilizing agonist Am J Physiol Gastrointest Liver Physiol, September 1, 2001; 281(3): G809 - G815. [Abstract] [Full Text] [PDF]
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