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PubMed2005

Plants, symbiosis and parasites: a calcium signalling connection.

A unique family of protein kinases has evolved with regulatory domains containing sequences that are related to Ca(2+)-binding EF-hands. In this family, the archetypal Ca(2+)-dependent protein kinases (CDPKs) have been found in plants and some protists, including the malarial parasite, Plasmodium falciparum. Recent genetic evidence has revealed isoform-specific functions for a CDPK that is essential for Plasmodium berghei gametogenesis, and for a related chimeric Ca(2+) and calmodulin-dependent protein kinase (CCaMK) that is essential to the formation of symbiotic nitrogen-fixing nodules in plants. In Arabidopsis thaliana, the analysis of 42 isoforms of CDPK and related kinases is expected to delineate Ca(2+) signalling pathways in all aspects of plant biology.

Animals↗
PubMed2006

Analysis of Nod-factor-induced calcium signaling in root hairs of symbiotically defective mutants of Lotus japonicus.

Nodulation (Nod)-factor signaling molecules are essential for rhizobia to initiate the nitrogen-fixing symbiotic interaction with legumes. Using a dual dye ratiometric calcium imaging technique, we have shown that 10 nM Nod factor added to roots of Lotus japonicus seedlings induces an intracellular calcium increase (calcium flux) that precedes oscillations in intracellular calcium (calcium spiking). The calcium flux was not observed with 1 or 0.1 nM Nod factor, which did induce calcium spiking. The calcium flux was variable in timing of initiation and duration and was observed in approximately half of the root hairs examined. Representatives from 11 complementation groups of symbiotically defective mutants were analyzed for the calcium flux. Mutants from four groups (sym6, ccamk, sym35, and nin) which retained calcium spiking all showed a normal calcium flux. Two classes of mutants (nfr1 and nfr5) lacked both calcium influx and calcium spiking, whereas five classes of mutants (symRK, castor, pollux, nup133, and sym24) defective for calcium spiking retained a calcium flux. There was no correlation between calcium spiking and induction of root hair deformation by Nod factor. We propose that increased bacterial numbers within infection foci in root hairs leads to accumulation of Nod factor to sufficient levels to activate the calcium flux, and this may drive infection thread growth.

Alphaproteobacteria↗
PubMed2005

Activation of chondrocytes calcium signalling by dynamic compression is independent of number of cycles.

Mechanical loading is necessary for the development and maintenance of healthy articular cartilage through the control of extracellular matrix synthesis and catabolism. However, the underlying process of chondrocyte mechanotransduction remains unclear. This study examined the influence of cyclic compression on intracellular calcium (Ca(2+)) signalling within isolated articular chondrocytes cultured in agarose constructs. A validated experimental system was developed for applying controlled cyclic cell deformation. Cell-agarose constructs were subjected to 1Hz cyclic compression between 0 and 10% gross strain for 1, 10, 100 or 300 cycles. The cells were subsequently visualised for 300s in the unstrained state using confocal microscopy and the Ca(2+) indicator, Fluo-4 AM. Within unloaded control constructs, a sub-population of approximately 50% of chondrocytes exhibited characteristic spontaneous Ca(2+) transients each lasting approximately 40-60s. Cyclic compression, for only 1 cycle, significantly up-regulated the percentage of cells exhibiting Ca(2+) transients in the subsequent 5min period (p<0.05). Increasing the number of cycles to 10 or 100 had no additional effect. The up-regulated Ca(2+) signalling was maintained for up to 5min before returning to basal levels. By contrast, 300 cycles were followed by Ca(2+) signalling that was not significantly different from that in unloaded controls. However, this response was shown to be due to the increased time following the start of compression. In conclusion, this study indicates that chondrocyte Ca(2+) signalling is stimulated by dynamic compression, probably mediated by cyclic cell deformation. The overall response appears to be independent of the number of cycles or duration of cyclic compression. The sustained up-regulation of Ca(2+) signalling after 1, 10 or 100 cycles suggests the involvement of an autocrine-paracrine signalling mechanism. Furthermore, the reduced response following 300 cycles indicates a possible receptor desensitisation mechanism. Therefore, Ca(2+) signalling may be part of a mechanotransduction pathway through which chondrocyte populations can modulate their metabolic activity in response to changing mechanical stimuli.

Animals↗
PubMed1999

Calcium signaling in cold cells studied in cultured dorsal root ganglion neurons.

Thermosensitive cold cells were identified in cultured dorsal root ganglion neurons from newborn rats. The neurons were loaded with a calcium indicator, Fura-PE3, and the change in intracellular Ca2+ concentration ([Ca2+]i) of the neurons was measured with microfluorimetry. Thirteen per cent of the cells responded to the cold stimulation. The diameter of the responder cells was 16.3+/-3.2 microm (mean+/-S.D., n = 25). The lowering of the temperature from 35 degrees C to 20 degrees C increased [Ca2+]i from 59.6+/-10.6 nM to 203.4+/-14.8 nM (n = 25). The [Ca2+]i response was dependent on the intensity of the cold stimulation. The depletion of extracellular Ca2+ diminished the Ca2+ elevation. However, a Na(+)-free condition did not influence the response. We concluded that the cold stimulation opens Ca2(+)-permeable channels in putative cold cells from dorsal root ganglion neurons.

Animals↗
PubMed2000

Acute stress induced modifications of calcium signaling in learned helpless rats.

Previous reports have demonstrated reduced elevations of free intracellular calcium concentration in blood cells of depressed patients after various stimuli. Therefore, a disturbance of intracellular calcium (Ca2+) homeostasis has been postulated to be involved in the pathophysiology of mood disorders. It was the aim of the present study to investigate whether Ca2+ signaling was affected in spleen T-lymphocytes of rats submitted to a learned helplessness paradigm, an animal model of depression with a high level of construct, face and predictive validity. In addition, we tested for effects of acute stress on the Ca2+ signaling in helpless rats, as compared to non-stressed rats. It was found that mitogen-induced Ca2+ signaling only tended to be reduced in helpless rats. However, when helpless rats were submitted to acute immobilization stress, Ca2+ signaling appeared to be significantly blunted, whereas the same stressor did not affect Ca2+ signaling in the non-helpless control rats. These acute stress-induced differences in Ca2+ signaling were not paralleled by a differential increase in plasma corticosterone. It is hypothesized that blunted Ca2+ signaling, as assessed in spleen T-lymphocytes of helpless rats, may be a correlate of the increased vulnerability of helpless rats to acute stressors.

Animals↗
PubMed2003

Casein binds to the cell membrane and induces intracellular calcium signals in the enteroendocrine cell: a brief communication.

Dietary protein but not amino acids stimulates cholecystokinin (CCK) secretion in rat mucosal cells. However, the dietary protein sensory mechanisms and the intracellular signal pathway in the enteroendocrine cells have not yet been clarified. The relationship between dietary protein binding to cell membrane and intracellular calcium responses were examined in the CCK-producing enteroendocrine cell line STC-1. The binding of solubilized STC-1 cell membrane to proteins was analyzed using a surface plasmon resonance sensor. Intracellular calcium concentrations of STC-1 cell suspensions loaded with Fura-2 AM were measured using a spectrafluorophotometer system with continuous stirring. Intracellular calcium concentrations in STC-1 cells were increased by exposure to alpha-casein or casein sodium, but not to bovine serum albumin. Solubilized STC-1 membranes bound to alpha-casein and casein sodium but did not bind to bovine serum albumin. alpha-Casein demonstrated higher membrane binding and intracellular calcium stimulating activities than casein sodium. Thus, protein binding to the STC-1 cell membrane and intracellular calcium responses were correlated. Intracellular calcium responses to alpha-casein were suppressed by an L-type calcium channel blocker. These results suggest that casein, a dietary protein, binds to a putative receptor on the CCK-producing enteroendocrine cell membrane and elicits the subsequent intracellular calcium response via an L-type calcium channel.

Animals↗
PubMed2000

Calcium signaling and annexins.

The annexins, are a family of calcium ion (Ca2+)-binding proteins whose physiological functions are poorly understood. Although many diverse functions have been proposed for these proteins, such as in vesicle trafficking, this review focuses on their proposed roles as Ca2+ or other ion channels, or as intracellular ion channel regulators. Such ideas are founded mainly on in vitro and structural analyses, but there is increasing evidence that at least some members of this protein family may indeed play a part in intracellular Ca2+ signaling by acting both as atypical ion channels and as modulators of ion channel activity. This review first introduces the annexin family, then discusses intracellular localization, developmental regulation, and modes of membrane association of annexins, which suggest roles in Ca2+ homeostasis. Finally, it examines the structural and electrophysiological data that argue for key roles for annexins in the control of ion fluxes.

Animals↗
PubMed1999

Calcium signaling molecules in human cerebellum at midgestation and in ataxia.

A fundamental question in brain development is how neurons make the precise topographic connections necessary for function. The hypothesis that transient expression of calcium (Ca2+) signaling molecules may have a role in this process was tested by studying human cerebella at midgestation. In addition, four adult brains, two controls and two from patients with ataxia, were studied as well. The temporal and spatial distribution of intracellular Ca2+ channel/receptors, inositol trisphosphate receptor type 1 (IP3R1) and ryanodine receptor (RyR) and three Ca2+ binding proteins were examined with immunocytochemical methods. A positive immune reaction with all markers of Ca2+ signaling was found in the Purkinje cell layer starting from 17 g.w. (gestational weeks), the youngest age studied. The immune reactions were not homogeneous throughout the extent of the Purkinje cell layer, but instead displayed a 'patchy' appearance in all intrauterine stages. In the adult cerebellum the expression of Ca2+ signaling molecules was homogenous. In the two cerebella obtained from patients suffering from ataxia, a several-fold reduction of immunostaining with IP3R1 was found. Our findings suggest that transient and differential mobilization of intracellular Ca2+ in seemingly homogenous neuronal types may play a role in development of highly organized projection maps of the cerebellar cortex. Moreover, lack of IP3R1 in the diseased brains suggests that internal stores of Ca2+ play an important role in normal function of the cerebellum.

Adult↗
PubMed2005

Epidermal growth factor receptor downregulation in cultured bovine cumulus cells: reconstitution of calcium signaling and stimulated membrane permeabilization.

Cumulus cell-oocyte complexes (COCs), cultured in vitro, are competent for maturation and fertilization. Inclusion of epidermal growth factor (EGF) in the COC culture medium enhances in vitro maturation and subsequent embryonic development. It has been shown that isolated COCs exposed to EGF respond with a prolonged and pulsatile release of Ca2+ into the extra-cellular medium and that cumulus cells (CCs) of complexes exhibit both a slow rise in intracellular [Ca2+] ([Ca2+]i) and plasma membrane permeabilization in response to EGF. These unusual signaling responses were examined in isolated, cultured bovine CCs. Few individual CCs showed [Ca2+]i increases; the lack of response was found to be due to decrease of expression of endogenous EGF receptors after dissociation. CCs transfected with a human EGF receptor-GFP fusion protein showed robust, prolonged, EGF-stimulated [Ca2+]i elevations characteristic of CC responses in intact COCs. Many CCs that responded to EGF stimulation with a [Ca2+]i rise also released entrapped fura-2 dye at the peak of the [Ca2+]i response, suggesting that CC permeabilization and death follows activation of the EGF receptor. The [Ca2+]i elevation due to EGF stimulation and subsequent membrane permeabilization was shown to be mediated by the inositol triphosphate signaling pathway.

Animals↗
PubMedDate not supplied

Wnt and calcium signaling: beta-catenin-independent pathways.

Wnt signaling is a complex pathway in which beta-catenin is typically viewed as a central mediator. However, within the past 15 years, at least three Wnt-mediated pathways have been proposed that function independent of beta-catenin. One pathway involves activation of calcium/calmodulin-dependent kinase II (CamKII) and protein kinase C (PKC). Another includes recruitment of heterotrimeric GTP-binding proteins to activate phospholipase C (PLC) and phosphodiesterase (PDE). Lastly, a pathway similar to the planar cell polarity (PCP) pathway in Drosophila has been identified that activates the Jun-N-terminal kinase (JNK) and, perhaps, small GTP-binding proteins. Calcium has been implicated as an important second messenger in all of these pathways. This review will focus on the role of calcium in Wnt signaling and, as a consequence, provide a limited overview of beta-catenin-independent Wnt signaling.

Animals↗
PubMed2001

Extracellular NAD(+) induces calcium signaling and apoptosis in human osteoblastic cells.

ADP-ribosyl cyclase/CD38 is a bifunctional enzyme that catalyzes at its ectocellular domain the synthesis from NAD(+) (cyclase) and the hydrolysis (hydrolase) of the calcium-mobilizing second messenger cyclic ADP ribose (cADPR). Furthermore, CD38 mediates cADPR influx inside a number of cells, thereby inducing Ca(2+) mobilization. Intracellularly, cADPR releases Ca(2+) from ryanodine-sensitive pools, thus activating several Ca(2+)-dependent functions. Among these, the inhibition of osteoclastic-mediated bone resorption has been demonstrated. We found that HOBIT human osteoblastic cells display ADP-ribosyl cyclase activity and we examined the effects of CD38 stimulation on osteoblasts function. Extracellular NAD(+) induced elevation of cytosolic calcium due to both Ca(2+) influx from the extracellular medium and Ca(2+) release from ryanodine-sensitive intracellular stores. Culturing these cells in the presence of NAD(+) caused a complete growth arrest with a time-dependent decrease of cell number and the appearance of apoptotic nuclei. The first changes could be observed after 24 h of treatment and became fully evident after 72-96 h. We propose a role of extracellular NAD(+) in bone homeostatic control.

ADP-ribosyl Cyclase↗
PubMed2000

Effects of antioxidants on calcium signal induced by cholecystokinin in mouse pancreatic acinar cells.

Digital imaging fluorescence microscopy was used to study the effect of two antioxidants, N-acetyl-cysteine (NAC) and glutathione, on the cytosolic free calcium concentration ([Ca2+]i) induced by cholecystokinin-octapeptide (CCK-8) of mouse pancreatic acinar cells. When acinar cells were preincubated with either NAC or glutathione, subsequent stimulation with CCK-8 in the presence of each antioxidant had no significant effect on the typical pattern of [Ca2+]i transient evoked by the gastrointestinal hormone. However, application of NAC to acinar cells pretreated for 60 min with the same antioxidant, strongly blocked the oscillatory pattern initiated by CCK-8, inhibiting both amplitude and frequency of calcium oscillations. By contrast, glutathione had no effect on the oscillatory pattern evoked by CCK-8. The present results allow us to speculate that during [Ca2+]i oscillation there is a production of oxidants that facilitate oscillations by enhancing release of calcium from internal stores.

Acetylcysteine↗
PubMed1994

Spatial changes in calcium signaling during the establishment of neuronal polarity and synaptogenesis.

Calcium imaging techniques were used to obtain a clear although indirect evidence about the distribution of functional glutamate receptors of NMDA and non-NMDA type in cultured hippocampal neurons during establishment of polarity and synaptogenesis. Glutamate receptors were expressed and were already functional as early as one day after plating. At this stage NMDA and non-NMDA receptors were distributed in all plasmalemmal areas. During the establishment of neuronal polarity, responses to either types of glutamate receptors became restricted to the soma and dendrites. Compartmentalization of glutamate receptors occurred at stages of development when synaptic vesicles were already fully segregated to the axon. Formation of synapses was accompanied by a further redistribution of receptors, which segregated to synapse-enriched portions of dendrites. Receptor compartmentalization and dendritic redistribution as well as accumulation of synaptic vesicles at synaptic sites occurred also in neurons cultured in the presence of either the sodium channel blocker tetrodotoxin or glutamate receptor antagonists. These results indicate that signals generated by neuronal electrical activity or receptor activation are not involved in the establishment of neuronal polarity and synaptogenesis.

Animals↗
PubMed1990

Luteinizing hormone but not endothelin can induce a calcium signal in the chicken granulosa cell.

Using the fluorescent calcium-indicator Indo-1 we demonstrated a rapid transient increase of cytosolic calcium level in dispersed chicken granulosa cells in response to 10-100 ng/ml ovine luteinizing hormone (LH). The magnitude of the signal was dose-dependent, it lasted for about 30 seconds and could be provoked even when the extracellular calcium had been chelated by EGTA. A high, 100 ng/ml concentration of LH abolished completely the responsiveness of these cells to a second exposure to the agonist. We conclude, that LH can mobilize calcium ions from internal store(s) via a desenzitizable mechanism. Finally, endothelin--a vasoactive peptide with Ca2(+)-mobilizing activity in glomerulosa cells--was shown to have no effect on the concentration of cytosolic Ca2+ in chicken granulosa cells.

Animals↗