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Cytosolic Free Ca2+ (cytosolic + free_ca2+)
Terms modified by Cytosolic Free Ca2+ Selected AbstractsProducts of tryptophan catabolism induce Ca2+ release and modulate the cell cycle of Plasmodium falciparum malaria parasitesJOURNAL OF PINEAL RESEARCH, Issue 3 2005Flávio H. Beraldo Abstract:, Intraerythrocytic malaria parasites develop in a highly synchronous manner. We have previously shown that the host hormone melatonin regulates the circadian rhythm of the rodent malaria parasite, Plasmodium chabaudi, through a Ca2+ -based mechanism. Here we show that melatonin and other molecules derived from tryptophan, i.e. N -acetylserotonin, serotonin and tryptamine, also modulate the cell cycle of human malaria parasite P. falciparum by inducing an increase in cytosolic free Ca2+. This occurs independently of the extracellular Ca2+ concentration, indicating that these molecules induce Ca2+ mobilization from intracellular stores in the trophozoite. This in turn leads to an increase in the proportion of schizonts. The effects of the indolamines in increasing cytosolic free Ca2+ and modulating the parasite cell cycle are both abrogated by an antagonist of the melatonin receptor, luzindole, and by the phospholipase inhibitor, U73122. [source] Protein kinase C-, mediates von Willebrand factor secretion from endothelial cells in response to vascular endothelial growth factor (VEGF) but not histamineJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 11 2008O. LORENZI Summary.,Background:,Vascular endothelial growth factor (VEGF) and histamine induce von Willebrand factor (VWF) release from vascular endothelial cells. Protein kinase C (PKC) is involved in the control of exocytosis in many secretory cell types. Objectives:,We investigated the role of PKC and the interactions between PKC and Ca2+ signaling in both VEGF-induced and histamine-induced VWF secretion from human umbilical vein endothelial cells (HUVECs). Results:,Several PKC inhibitors (staurosporine, Ro31-8220, myristoylated PKC peptide inhibitor and Go6983) block VEGF-induced but not histamine-induced VWF secretion. PKC-, and novel PKCs (PKC-,, PKC-,, and PKC-,), but not PKC-,, are expressed in HUVECs. Both VEGF and histamine activate PKC-,. However, gene inactivation experiments using small interfering RNA indicate that PKC-, (but not PKC-,) is involved in the regulation of VEGF-induced but not histamine-induced secretion. Both VEGF and histamine induce a rise in cytosolic free Ca2+ ([Ca2+]c), but the response to VEGF is weaker and even absent in a significant subset of cells. Furthermore, VEGF-induced secretion is largely preserved when the rise in [Ca2+]c is prevented by BAPTA-AM. Conclusions:,Our study identifies striking agonist specificities in signal,secretion coupling. Histamine-induced secretion is dependent on [Ca2+]c but not PKC, whereas VEGF-induced secretion is largely dependent on PKC-, and significantly less on [Ca2+]c. Our data firmly establish the key role of PKC-, in VEGF-induced VWF release, but suggest that a third, VEGF-specific, signaling intermediate is required as a PKC-, coactivator. [source] Molecular mechanisms of apoptosis induced by magnolol in colon and liver cancer cellsMOLECULAR CARCINOGENESIS, Issue 2 2001Shyr-Yi Lin Abstract Magnolol has been reported to have anticancer activity. In this study we found that treatment with 100 ,m magnolol induced apoptosis in cultured human hepatoma (Hep G2) and colon cancer (COLO 205) cell lines but not in human untransformed gingival fibroblasts and human umbilical vein endothelial cells. Our investigation of apoptosis in Hep G2 cells showed a sequence of associated intracellular events that included (a) increased cytosolic free Ca2+; (b) increased translocation of cytochrome c (Cyto c) from mitochondria to cytosol; (c) activation of caspase 3, caspase 8, and caspase 9; and (d) downregulation of bcl-2 protein. Pretreatment of the cells with the phospholipase C inhibitor 1-[6-[[(17,)-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1 H -pyrrole-2,5-dione (U73122) or the intracellular chelator of Ca2+ 1,2-bis(2-aminophenoxy)ethane- N,N,N,,N, -tetraacetic acid acetoxymethyl ester (BAPTA/AM) inhibited the subsequent magnolol augmentation of [Ca2+]i and also the activation of caspase-8 and caspase-9, so that the occurrence of apoptosis in those cells was greatly reduced. Pretreatment of the cells with ZB4 (which disrupts the Fas response mechanism) also decreased the subsequent magnolol-induced caspase-8 activation and reduced the occurrence of apoptosis. We interpreted these findings to indicate that the above-listed sequence of intracellular events led to the apoptosis seen in Hep G2 cells and that [Ca2+]i, Cyto c, and Fas function as intracellular signals to coordinate those events. © 2001 Wiley-Liss, Inc. [source] Unravelling response-specificity in Ca2+ signalling pathways in plant cellsNEW PHYTOLOGIST, Issue 1 2001Jason J. Rudd Summary Considerable advances have been made, both in the technologies available to study changes in intracellular cytosolic free Ca2+ ([Ca2+]i), and in our understanding of Ca2+ signalling cascades in plant cells, but how specificity can be generated from such a ubiquitous component as Ca2+ is questionable. Recently the concept of ,Ca2+ signatures' has been formulated; tight control of the temporal and spatial characteristics of alterations in [Ca2+]i signals is thought to be responsible, at least in part, for the specificity of the response. However, the way in which Ca2+ signatures are decoded, which depends on the nature and location of the targets of the Ca2+ signals, has received little attention. In a few key systems, progress is being made on how diverse Ca2+ signatures might be transduced within cells in response to specific signals. Valuable pieces of the signal-specificity puzzle are being put together and this is illustrated here using some key examples; these emphasize the global importance of Ca2+ -mediated signal-transduction cascades in the responses of plants to a wide diversity of extracellular signals. However, the way in which signal specificity is encoded and transduced is still far from clear. [source] NaCl-induced changes in cytosolic free Ca2+ in Arabidopsis thaliana are heterogeneous and modified by external ionic compositionPLANT CELL & ENVIRONMENT, Issue 8 2008FRANCES E. TRACY ABSTRACT Increases in cytosolic free Ca2+ ([Ca2+]cyt) are common to many stress-activated signalling pathways, including the response to saline environments. We have investigated the nature of NaCl-induced [Ca2+]cyt signals in whole Arabidopsis thaliana seedlings using aequorin. We found that NaCl-induced increases in [Ca2+]cyt are heterogeneous and mainly restricted to the root. Both the concentration of NaCl and the composition of the solution bathing the root have profound effects on the magnitude and dynamics of NaCl-induced increases in [Ca2+]cyt. Alteration of external K+ concentration caused changes in the temporal and spatial pattern of [Ca2+]cyt increase, providing evidence for Na+ -induced Ca2+ influx across the plasma membrane. The effects of various pharmacological agents on NaCl-induced increases in [Ca2+]cyt indicate that NaCl may induce influx of Ca2+ through both plasma membrane and intracellular Ca2+ -permeable channels. Analysis of spatiotemporal [Ca2+]cyt dynamics using photon-counting imaging revealed additional levels of complexity in the [Ca2+]cyt signal that may reflect the oscillatory nature of NaCl-induced changes in single cells. [source] Plant extracellular ATP signalling by plasma membrane NADPH oxidase and Ca2+ channelsTHE PLANT JOURNAL, Issue 6 2009Vadim Demidchik Summary Extracellular ATP regulates higher plant growth and adaptation. The signalling events may be unique to higher plants, as they lack animal purinoceptor homologues. Although it is known that plant cytosolic free Ca2+ can be elevated by extracellular ATP, the mechanism is unknown. Here, we have studied roots of Arabidopsis thaliana to determine the events that lead to the transcriptional stress response evoked by extracellular ATP. Root cell protoplasts were used to demonstrate that signalling to elevate cytosolic free Ca2+ is determined by ATP perception at the plasma membrane, and not at the cell wall. Imaging revealed that extracellular ATP causes the production of reactive oxygen species in intact roots, with the plasma membrane NADPH oxidase AtRBOHC being the major contributor. This resulted in the stimulation of plasma membrane Ca2+ -permeable channels (determined using patch-clamp electrophysiology), which contribute to the elevation of cytosolic free Ca2+. Disruption of this pathway in the AtrbohC mutant impaired the extracellular ATP-induced increase in reactive oxygen species (ROS), the activation of Ca2+ channels, and the transcription of the MAP kinase3 gene that is known to be involved in stress responses. This study shows that higher plants, although bereft of purinoceptor homologues, could have evolved a distinct mechanism to transduce the ATP signal at the plasma membrane. [source] Dynamics of ionic activities in the apoplast of the sub-stomatal cavity of intact Vicia faba leaves during stomatal closure evoked by ABA and darknessTHE PLANT JOURNAL, Issue 3 2000Hubert H. Felle Summary Stomatal movement is accomplished by changes in the ionic content within guard cells as well as in the cell wall of the surrounding stomatal pore. In this study, the sub-stomatal apoplastic activities of K+, Cl,, Ca2+ and H+ were continuously monitored by inserting ion-selective micro-electrodes through the open stomata of intact Vicia faba leaves. In light-adapted leaves, the mean activities were 2.59 mm (K+), 1.26 mm (Cl,), 64 µm (Ca2+) and 89 µm (H+). Stomatal closure was investigated through exposure to abscisic acid (ABA), sudden darkness or both. Feeding the leaves with ABA through the cut petiole initially resulted in peaks after 9,10 min, in which Ca2+ and H+ activities transiently decreased, and Cl, and K+ activities transiently increased. Thereafter, Ca2+, H+ and Cl, activities completely recovered, while K+ activity approached an elevated level of around 10 mm within 20 min. Similar responses were observed following sudden darkness, with the difference that Cl, and Ca2+ activities recovered more slowly. Addition of ABA to dark-adapted leaves evoked responses of Cl, and Ca2+ similar to those observed in the light. K+ activity, starting from its elevated level, responded to ABA with a transient increase peaking around 16 mm, but then returned to its dark level. During stomatal closure, membrane potential changes in mesophyll cells showed no correlation with the K+ kinetics in the sub-stomatal cavity. We thus conclude that the increase in K+ activity mainly resulted from K+ release by the guard cells, indicating apoplastic compartmentation. Based on the close correlation between Cl, and Ca2+ changes, we suggest that anion channels are activated by a rise in cytosolic free Ca2+, a process which activates depolarization-activated K+ release channels. [source] | |||||||||||||