The Impact of Vitamin D3 Supplementation on Mechanisms of Cell Calcium Signaling in Chronic Kidney Disease
Intracellular calcium concentration in peripheral blood mononuclear cells (PBMCs) of patients with chronic kidney disease (CKD) is significantly increased, and the regulatory mechanisms maintaining cellular calcium homeostasis are impaired. The purpose of this study was to examine the effect of vita...
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Online Access: | http://dx.doi.org/10.1155/2015/807673 |
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doaj-83bc86f9764d47ef9f1e9447673ee39c2020-11-24T20:40:43ZengHindawi LimitedBioMed Research International2314-61332314-61412015-01-01201510.1155/2015/807673807673The Impact of Vitamin D3 Supplementation on Mechanisms of Cell Calcium Signaling in Chronic Kidney DiseaseIngrid Lajdova0Viera Spustova1Adrian Oksa2Zuzana Kaderjakova3Dusan Chorvat4Marcela Morvova5Libusa Sikurova6Alzbeta Marcek Chorvatova7Department of Clinical and Experimental Pharmacology, Faculty of Medicine, Slovak Medical University, 833 03 Bratislava, SlovakiaDepartment of Clinical and Experimental Pharmacology, Faculty of Medicine, Slovak Medical University, 833 03 Bratislava, SlovakiaDepartment of Clinical and Experimental Pharmacology, Faculty of Medicine, Slovak Medical University, 833 03 Bratislava, SlovakiaDepartment of Nuclear Physics and Biophysics, Faculty of Mathematics, Physics and Informatics, Comenius University, 833 03 Bratislava, SlovakiaDepartment of Biophotonics, International Laser Centre, 833 03 Bratislava, SlovakiaDepartment of Nuclear Physics and Biophysics, Faculty of Mathematics, Physics and Informatics, Comenius University, 833 03 Bratislava, SlovakiaDepartment of Nuclear Physics and Biophysics, Faculty of Mathematics, Physics and Informatics, Comenius University, 833 03 Bratislava, SlovakiaDepartment of Biophotonics, International Laser Centre, 833 03 Bratislava, SlovakiaIntracellular calcium concentration in peripheral blood mononuclear cells (PBMCs) of patients with chronic kidney disease (CKD) is significantly increased, and the regulatory mechanisms maintaining cellular calcium homeostasis are impaired. The purpose of this study was to examine the effect of vitamin D3 on predominant regulatory mechanisms of cell calcium homeostasis. The study involved 16 CKD stages 2-3 patients with vitamin D deficiency treated with cholecalciferol 7000–14000 IU/week for 6 months. The regulatory mechanisms of calcium signaling were studied in PBMCs and red blood cells. After vitamin D3 supplementation, serum concentration of 25(OH)D3 increased (P<0.001) and [Ca2+]i decreased (P<0.001). The differences in [Ca2+]i were inversely related to differences in 25(OH)D3 concentration (P<0.01). Vitamin D3 supplementation decreased the calcium entry through calcium release activated calcium (CRAC) channels and purinergic P2X7 channels. The function of P2X7 receptors was changed in comparison with their baseline status, and the expression of these receptors was reduced. There was no effect of vitamin D3 on P2X7 pores and activity of plasma membrane Ca2+-ATPases. Vitamin D3 supplementation had a beneficial effect on [Ca2+]i decreasing calcium entry via CRAC and P2X7 channels and reducing P2X7 receptors expression.http://dx.doi.org/10.1155/2015/807673 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ingrid Lajdova Viera Spustova Adrian Oksa Zuzana Kaderjakova Dusan Chorvat Marcela Morvova Libusa Sikurova Alzbeta Marcek Chorvatova |
spellingShingle |
Ingrid Lajdova Viera Spustova Adrian Oksa Zuzana Kaderjakova Dusan Chorvat Marcela Morvova Libusa Sikurova Alzbeta Marcek Chorvatova The Impact of Vitamin D3 Supplementation on Mechanisms of Cell Calcium Signaling in Chronic Kidney Disease BioMed Research International |
author_facet |
Ingrid Lajdova Viera Spustova Adrian Oksa Zuzana Kaderjakova Dusan Chorvat Marcela Morvova Libusa Sikurova Alzbeta Marcek Chorvatova |
author_sort |
Ingrid Lajdova |
title |
The Impact of Vitamin D3 Supplementation on Mechanisms of Cell Calcium Signaling in Chronic Kidney Disease |
title_short |
The Impact of Vitamin D3 Supplementation on Mechanisms of Cell Calcium Signaling in Chronic Kidney Disease |
title_full |
The Impact of Vitamin D3 Supplementation on Mechanisms of Cell Calcium Signaling in Chronic Kidney Disease |
title_fullStr |
The Impact of Vitamin D3 Supplementation on Mechanisms of Cell Calcium Signaling in Chronic Kidney Disease |
title_full_unstemmed |
The Impact of Vitamin D3 Supplementation on Mechanisms of Cell Calcium Signaling in Chronic Kidney Disease |
title_sort |
impact of vitamin d3 supplementation on mechanisms of cell calcium signaling in chronic kidney disease |
publisher |
Hindawi Limited |
series |
BioMed Research International |
issn |
2314-6133 2314-6141 |
publishDate |
2015-01-01 |
description |
Intracellular calcium concentration in peripheral blood mononuclear cells (PBMCs) of patients with chronic kidney disease (CKD) is significantly increased, and the regulatory mechanisms maintaining cellular calcium homeostasis are impaired. The purpose of this study was to examine the effect of vitamin D3 on predominant regulatory mechanisms of cell calcium homeostasis. The study involved 16 CKD stages 2-3 patients with vitamin D deficiency treated with cholecalciferol 7000–14000 IU/week for 6 months. The regulatory mechanisms of calcium signaling were studied in PBMCs and red blood cells. After vitamin D3 supplementation, serum concentration of 25(OH)D3 increased (P<0.001) and [Ca2+]i decreased (P<0.001). The differences in [Ca2+]i were inversely related to differences in 25(OH)D3 concentration (P<0.01). Vitamin D3 supplementation decreased the calcium entry through calcium release activated calcium (CRAC) channels and purinergic P2X7 channels. The function of P2X7 receptors was changed in comparison with their baseline status, and the expression of these receptors was reduced. There was no effect of vitamin D3 on P2X7 pores and activity of plasma membrane Ca2+-ATPases. Vitamin D3 supplementation had a beneficial effect on [Ca2+]i decreasing calcium entry via CRAC and P2X7 channels and reducing P2X7 receptors expression. |
url |
http://dx.doi.org/10.1155/2015/807673 |
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