scholarly journals Benzothiazepine CGP37157 and Its Isosteric 2′-Methyl Analogue Provide Neuroprotection and Block Cell Calcium Entry

2012 ◽  
Vol 3 (7) ◽  
pp. 519-529 ◽  
Author(s):  
Laura González-Lafuente ◽  
Javier Egea ◽  
Rafael León ◽  
Francisco J. Martínez-Sanz ◽  
Leticia Monjas ◽  
...  
Keyword(s):  
Calcium Entry ◽  
Cell Calcium

scholarly journals The Impact of Vitamin D3Supplementation on Mechanisms of Cell Calcium Signaling in Chronic Kidney Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Ingrid Lajdova ◽  
Viera Spustova ◽  
Adrian Oksa ◽  
Zuzana Kaderjakova ◽  
Dusan Chorvat ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Calcium Signaling ◽  
Calcium Homeostasis ◽  
Calcium Release ◽  
Calcium Entry ◽  
Regulatory Mechanisms ◽  
Cell Calcium ◽  
Crac Channels ◽  
The Impact

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 vitaminD3on 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 vitaminD3supplementation, serum concentration of 25(OH)D3increased (P<0.001) and[Ca2+]idecreased (P<0.001). The differences in[Ca2+]iwere inversely related to differences in 25(OH)D3concentration (P<0.01). VitaminD3supplementation decreased the calcium entry through calcium release activated calcium (CRAC) channels and purinergic P2X7channels. The function of P2X7receptors was changed in comparison with their baseline status, and the expression of these receptors was reduced. There was no effect of vitaminD3on P2X7pores and activity of plasma membrane Ca2+-ATPases. VitaminD3supplementation had a beneficial effect on[Ca2+]idecreasing calcium entry via CRAC and P2X7channels and reducing P2X7receptors expression.

Expression of polycystin-1 enhances endoplasmic reticulum calcium uptake and decreases capacitative calcium entry in ATP-stimulated MDCK cells

2005 ◽  
Vol 289 (3) ◽  
pp. F521-F530 ◽  
Author(s):  
K. M. Hooper ◽  
A. Boletta ◽  
G. G. Germino ◽  
Q. Hu ◽  
R. C. Ziegelstein ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Homeostasis ◽  
Mdck Cells ◽  
Fluid Secretion ◽  
Calcium Entry ◽  
Loss Of Function ◽  
Capacitative Calcium Entry ◽  
Endoplasmic Reticulum Calcium ◽  
Cell Calcium ◽  
Er Calcium

Autosomal dominant polycystic kidney disease (ADPKD) types 1 and 2 arise as a consequence of mutations in the PKD1 or PKD2 genes, encoding polycystins-1 and -2. Because loss of function of either of the polycystins leads to a very similar phenotype and the two proteins are known to interact, polycystins-1 and -2 are probably active in the same pathway. The way in which loss of either polycystin leads to the development of ADPKD remains to be established, but disturbances of cell calcium regulation are likely to play an important role. Here, we demonstrate that polycystin-1, heterologously expressed in Madin-Darby canine kidney cells, had a pronounced effect on intracellular calcium homeostasis. ATP-induced calcium responses in transfection control cells exhibited a double peak and relatively gradual return to baseline. By contrast, cells expressing heterologous polycystin-1 showed a brief, uniphasic peak and an accelerated rate of decay. Heterologously expressed polycystin-1 accelerated endoplasmic reticulum (ER) calcium reuptake and inhibited capacitative calcium entry; we found no effect of the protein on mitochondrial calcium buffering or plasma membrane calcium extrusion. We therefore propose that polycystin-1 accelerated the decay of the cell calcium response to ATP by upregulation of ER calcium reuptake and consequent minimization of the stimulus for capacitative calcium entry. It is possible that cellular dedifferentiation, fluid secretion, and proliferation might therefore arise in ADPKD as a consequence of disturbances in cytoplasmic and ER calcium homeostasis and aberrant capacitative calcium entry.

Insulin Inhibits Coronary Endothelial Cell Calcium Entry and Coronary Artery Relaxation

2001 ◽  
Vol 38 (6) ◽  
pp. 885-892 ◽  
Author(s):  
Quang-Kim Tran ◽  
Hiroshi Watanabe ◽  
Hong-Yen Le ◽  
Kazuhiko Takeuchi ◽  
Yuichi Hattori ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Coronary Artery ◽  
Calcium Entry ◽  
Cell Calcium

Renal effects of nicardipine, a calcium entry blocker, in hypertensive type II diabetic patients with nephropathy

Diabetes ◽  
1986 ◽  
Vol 35 (11) ◽  
pp. 1206-1214 ◽  
Author(s):  
T. Baba ◽  
T. Ishizaki ◽  
Y. Ido ◽  
K. Aoyagi ◽  
S. Murabayashi ◽  
...  
Keyword(s):  
Calcium Entry ◽  
Diabetic Patients ◽  
Calcium Entry Blocker ◽  
Type Ii ◽  
Renal Effects ◽  
Entry Blocker
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