Intracellular free Ca2+ is one of important biological signals regulating a number of cell functions. It has been discussed widely and extensively in several cell types during the past two decades. Attention has been paid to the Ca2+ transportation in mesenchymal stem cells in recent years as mesenchymal stem cells have gained considerable interest due to their potential for cell replacement therapy and tissue engineering. In this paper, roles of intracellular Ca2+ oscillations and its transporters in mesenchymal stem cells have been reviewed., B. Ye., and Obsahuje bibliografii a bibliografické odkazy
Experimental and epidemiological studies suggest that calcium intake is inversely related to weight gain. Calcium of dairy origin has been shown to be more effective in promoting weight loss. However, clinical studies yielded controversial results concerning the role of calcium intake in weight change. The aim of this study was to ascertain whether the addition of calcium can affect the outcome of 3-week weight management (WM) with a hypocaloric diet characterized by a decreased calcium intake. Overweight/obese women (n=67; BMI 32.2±4.1 kg/m2; age 49.1±12.1 years) underwent a 4-week comprehensive WM program. WM included a 7 MJ/day diet resulting in a stable weight during the first week and a 4.5 MJ/day diet with mean daily calcium intake 350 mg during the second to fourth week. Participants were divided into three age- and BMI-matched groups who received placebo or calcium (500 mg/day). Calcium was administered either as carbonate or calcium of dairy origin (Lactoval). There was no significant difference in weight loss in response to WM between the placebo-treated and calcium-treated groups. However, addition of calcium to the diet resulted in a lower hunger score in the Eating Inventory as well as a decrease in plasma resistin levels. Body composition measured by bioimpedance demonstrated that added calcium leads to preservation of fat-free mass. Nevertheless, a greater loss of fat-free mass in the placebo group might be partly due to a greater loss of water., K. Kabrnová-Hlavatá, V. Hainer, M. Gojová, P. Hlavatý, V. Kopský, J. Nedvídková, M. Kunešová, J. Pařízková, M. Wagenknecht, M. Hill, J. Drbohlav., and Obsahuje bibliografii a bibliografické odkazy
Previous data concerning the action of calcium (Ca) on gastric acid secretion (GAS) indicated that calcium ions increase GAS elicited by gastrin released through a vagal mechanism, and also by a direct effect on parietal cells. Our research showed that the stimulating effect of calcium on gastric acid secretion can be antagonized by verapamil administration, which reduces gastric acid secretion . In the present study we followed the effect induced by administration of calcium and Ca-chelating agents (disodium EDTA) on gastric acid secretion and on carbonic anhydrase (CA) activity. We selected two groups of healthy volunteers: Group I (n=21) received a single i.v. dose of CaCl2 (15 mg/kg b.w.), whereas Group II (n=22) received a single i.v. dose of disodium EDTA (5 mg/kg b.w.). We determined blood calcium before and after treatment, gastric acid secretion at 2 hours, erythrocyte CA II activity, and CA IV activity in membrane parietal cells, which were isolated from gastric mucosa obtained by endoscopic biopsy. Assessment of carbonic anhydrase activity was achieved by the stopped-flow method. In Group I calcium administration increased blood calcium, HCl output, CA II and CA IV activity as compared to initial values. In Group II, disodium EDTA reduced blood calcium, HCl output, CA II and CA IV activity as compared to initial values. The results demonstrated that increased blood calcium and GAS values after calcium administration correlated with the increase of erythrocyte CA II and parietal cell CA IV activity, while disodium EDTA induced a reversed process. Our results also show that cytosolic CA II and membrane CA IV values are sensitive to calcium changes and they directly depend on these levels. Our data suggest that intra- and extracellular pH changes induced by carbonic anhydrase might account for the modulation of the physiological and pathological secretory processes in the organism., I. Puscas, M. Coltau, M. Baican, G. Domuta, A. Hecht., and Obsahuje bibliografii
We assessed the concentration of calcium, magnesium and creatinine in 2715 samples of the first morning urine. The investigation comprised the following age groups: children one, two, four, six, ten and thirteen years old, and groups of adults aged 18-35, 36-49, 50-65, 66-75, 76-85 and 86-93 years. The choice was made by random selection of participants of both sexes from diverse regions of the Czech Republic. We found the age to have a marked influence on the value of calcium, magnesium and creatinine, including urinary concentration ratios of calcium/creatinine and magnesium/crcatinine. The urinary calcium concentration was low both in the early and advanced age groups, while it reached peak values in subjects 18-35 years old. The urinary magnesium concentration was also age-dependent, with a maximum in children aged 4 years, and a subsequent decline with advancing age. The value of the ratio urinary calcium/creatinine and urinary magnesium/creatinine was highest in the youngest age group (1-4 years).
The lipid molecule, lysophosphatidylinositol (LPI), is hypothesis ed to form part of a novel lipid signalling system that involves the G protein- coupled receptor GPR55 and distinct in tracellular signalling cascades in endothelial cells. This work aimed to study the possible mechanisms involved in LPI -evoked cytosolic Ca 2+ mobilization in human brain microvascular endothelial cells. Changes in intracellular Ca 2+ concentrations were meas ured using cell population Ca 2+ assay. LPI evoked biphasic elevation of intracellular calcium concentration, a rapid phase and a sustained phase. The rapid phase was attenuated by the inhibitor of PLC (U 73122), inhibitor of IP 3 receptors, 2 -APB and the de pletor of endoplasmic reticulum Ca 2+ store, thapsigargin. The sustained phase, on the other hand, was enhanced by U 73122 and abolished by the RhoA kinase inhibitor, Y -27632. In conclusion, the Ca 2+ signal evoked by LPI is characterised by a rapid phase of Ca 2+ release from the endoplasmic reticulum, and requires activation of the PLC -IP 3 signalling pathway. The sustained phase mainly depends on RhoA kinase activation. LPI acts as novel lipid signalling molecule in endothelial cells, and elevation of cytosolic Ca 2+ triggered by it may present an important intracellular message required in gene expression and controlling of vascular tone., Y. M. Al Suleimani, C. R. Hiley., and Obsahuje bibliografii
Mosses are plants of simple anatomical structure and as they occur in habitats characterised not only by major changes in the concentrations of carbon dioxide, they suffer the stress of periodic water shortages or submergence in water. The condition of hypoxia (submergence in water or CaCl2 solution) prompted the increase in daily fluctuations in malate content, particularly in the gametophores of Polytrichum piliferum Hedw. No significant increases in daily fluctuations of citrate were found in the hypoxia and post-hypoxia conditions. Placing gametophores for 168 h in air with a concentration of CO2 at ∼ 350 μmol mol-1, and 21% of oxygen, after being submerged for 24 h in water, reduced the daily fluctuations of malate and citrate. Keeping the plants in these conditions for a long time (120-168 h) produced the increase in photosynthesis intensity in the gametophores of Mnium undulatum Hedw. and P. piliferum by 13% and 51%, respectively, when compared with plants submerged for 24 h. The intensity of respiration during post-hypoxia, however, was markedly lower compared with the intensity of the process recorded in hypoxia, particularly in the gametophores of P. piliferum. The increased daily fluctuations of malate and NAD(P)H in the studied species under hypoxia could constitute an important element of adaptive strategy to these conditions. and G. Rut, A. Rzepka, J. Krupa.
The effect of prenatal hypoxic stress on the cardiac contractile function and responsiveness to calcium was studied in rats during the perinatal period. Pregnant rats were exposed to intermittent high altitude hypoxia from day 14 to 18 of pregnancy. Foetal hearts (prenatal day 22) and the hearts of offsprings (days 1, 4 and 7) were isolated and perfused in the Langendorff mode. Developed force of contraction (DF) as well as the rate of force development and fall were measured a) at the Ca2+ concentration of 1.25 mmol.l-1, b) under increasing Ca2+ concentration (from 0.6 to 10.0 mmol.l-1). Body and heart weights were significantly smaller in hypoxic than in matched control rats starting from day 1. The contractile performance of hypoxic hearts did not differ from controls. Their inotropic response to increasing Ca2+ concentrations was, however, significantly reduced on prenatal day 22 and postnatal day 7. Our results suggest that prenatal maternal hypoxia affects the cardiac inotropic responsiveness to Ca2+ even postnatally.
Alterations of calcium handling and other second messenger cascades including protein kinase C (PKC) and A (PKA) were suggested to be responsible for abnormal vascular function in spontaneously hypertensive rats (SHR). However, the relative contribution of these pathways to vasoconstriction is still not completely understood. We investigated the effect of Ro 31-8220 (PKC inhibitor) and H89 (PKA inhibitor) on vasoconstriction induced by 120 mM KCl or by addition of 10 μM noradrenaline (NA) in isolated femoral arteries of control Wistar rats and SHR. Moreover, we investigated these responses in the presence and absence of Ca2+ ions in the incubation medium in order to assess the role of calcium influx in these contractions. We observed that while the vasoconstriction in the presence of calcium was not different between Wistar and SHR, the difference between constriction elicited by NA addition in the absence and presence of external calcium was larger in SHR. The inhibition of PKC had no effect on constrictions in SHR, but diminished constrictions in Wistar rats. PKA inhibition slightly enhanced constrictions in Wistar rats, but reduced them in the presence of calcium in SHR. We conclude that vasoconstriction elicited by adrenergic stimulation is more dependent on extracellular calcium influx in SHR compared to Wistar rats. Moreover, the activation of PKA contributes to this calcium-dependent vasoconstriction in SHR but not in Wistar. On the other hand, PKC activation seems to play a less important role in vasoconstriction in SHR than in Wistar rats., M. S. Bal ... [et al.]., and Obsahuje seznam literatury
We previously found that Endothelin-11-31 (ET-11-31) exhibited a pro-arrhythmogenic effect in isolated rat hearts. In this study, we further investigated the effects of ET-11-31 on a cell viability and observed [Ca2+]i in cultured cardiomyocytes. Cultured neonatal rat cardiomyocytes were treated with 0.1, 1, and 10 nM ET-11-31 for 24h in the presence or absence of ETA receptor antagonist (BQ123) or phosphoramidon, a NEP/ECE inhibitor. Cell injury was evaluated by supernatant lactate dehydrogenase (LDH) assay, superoxide dismutase (SOD activity, and malondialdehyde (MDA) content. Cell viability was assessed by MTT assay. [Ca2+]i was measured with Fluo-3/AM under a laser confocal microscope. 1) ET-11-31 dose-dependently increased LDH release and decreased cell viability. 2) LDH and MDA levels were significantly elevated and SOD activity decreased after administration of 1 nM ET-11-31 for 24h, and these changes were markedly attenuated by 1 uM BQ123. 3) Exposure to 10 nM ET-11-31 caused a continuous increase in [Ca2+]i to cultured beating cardiomyocytes and termination of [Ca2+]i transient within 6 min, and this change was reversed by 1 uM BQ123 and attenuated by 0.5 mM phosphoramidon. These results suggest that ET-11-31 could cause cell injury, and that the effect of ET-11-31 on [Ca2+]i transients is mainly mediated by ETA receptor and partially attributed to the conversion of ET-11-31 to ET-11-21., A.-J. Ren, X. Yuan, L. Lin, Y.-X. Pan, Y.-W. Qing, W.-J. Yuan., and Obsahuje bibliografii a bibliografické odkazy