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1
Content available remote

Effect of the intracellular calcium concentration chelator BAPTA acetoxy-methylester on action potential duration in canine ventricular myocytes

100%
Horvath B., Szentandrassy N., Veress R., Baranyai D., Kistamas K., Almassy J., Toth A., Magyar J., Banyasz T., Nanasi P. P.
Journal of Physiology and Pharmacology
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2018
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tom 69
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nr 1
2
Content available remote

Changes in intracellular calcium concentration influence beat-to-beat variability of action potential duration in canine ventricular myocytes

86%
Kistamas K., Szentandrassy, Hegyi B., Vaczi K., Ruzsnavszki F., Horvath B., Banyasz T., Nanasi P. P., Magyar J.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 1
3
Content available remote

The influence of insulin on calcium ion concentration during transduction of signals into neutrophils

72%
Demkow U., Winklewski P., Potapinska O., Popko K., Lipinska A., Wasik M.
Journal of Physiology and Pharmacology. Supplement
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2008
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tom 59
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nr 6
219-229
4

Alzheimer’s amyloid beta peptides disturb circadian oscillations of intracellular calcium concentration

72%
Kazmierczak A., Schmitt K., Grimm A., Strosznajder J. B., Eckert A.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr 1
It is postulated that disturbances in calcium homeostasis play an important role in pathogenesis of Alzheimer’s disease (AD). Changes of neuronal calcium concentration are responsible for the oxidative stress as well as altered metabolism and production of amyloid-beta peptides (Aβ). Aβ may further exacerbate calcium dysregulation, causing synaptic dysfunction, neurodegeneration and cognitive impairment. Recent data indicate that AD is associated with disturbances of circadian rhythm in the patients. However, till now nothing is known about the molecular mechanisms involved in AD-related circadian clock alterations. In our study we investigated the effect of Aβ peptides on the rhythmic oscillation of cytosolic and mitochondrial calcium levels. To investigate molecular clock mechanisms, the studies we carried out in human primary skin fibroblasts, a previously established experimental model. Our data showed circadian rhythm of calcium ions concentration in cytosol and mitochondria. Moreover we observed circadian oscillation of ROS formation and redox potential. Treatment with Aβ fibrils at the concentration of 0.5 µM disturbed cytosolic calcium oscillations and mitochondrial redox state. Studying mechanisms involved in this phenomenon indicated that Aβ did not affect ER calcium stores, but induced changes of calcium influx mediated by purinergic P2X7 receptor. The specific antagonist of P2X7 receptor Brillant Blue G abolished negative impact of Aβ and restored calcium circadian rhythm. Summarizing, our results indicate that Aβ may play a significant role in disturbances of circadian calcium oscillation, suggesting the importance of this phenomenon in ADrelated changes in biological clock. Supported by grants from Sciex 10. 258 to A.K. as well as Swiss National foundation (SNF No 310030_122572) and Synapsis Foundation to A.E.
5
Content available remote

Cigarette smoke extract influences intracellular calcium concentration in A549 cells

72%
Yoo Y.-M., Jung E.-M., Jeon B.-H., Tran D. N., Jeung E.-B.
Journal of Physiology and Pharmacology
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2020
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tom 71
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nr 5
6

Regulation of Ca2plus release from internal stores in cardiac and skeletal muscles

58%
Wrzosek A.
Acta Biochimica Polonica
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2000
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tom 47
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nr 3
It is widely accepted that Ca2+ is released from the sarcoplasmic reticulum by a specialized type of calcium channel, i.e., ryanodine receptor, by the process of Ca2+-induced Ca2+ release. This process is triggered mainly by dihydropyridine receptors, i.e., L-type (long lasting) calcium channels, directly or indirectly interacting with ryanodine receptor. In addition, multiple endogenous and exogenous compounds were found to modulate the activity of both types of calcium channels, ryanodine and dihydropyridine receptors. These compounds, by changing the Ca2+ transport activity of these channels, are able to influence intracellular Ca2+ homeostasis. As a result not only the overall Ca2+ concentration becomes affected but also spatial distribution of this ion in the cell. In cardiac and skeletal muscles the release of Ca2+ from internal stores is triggered by the same transport proteins, although by their specific isoforms. Concomitantly, heart and skeletal muscle specific regulatory mechanisms are different.
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