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At least 289 records · Page 16Linked to original sources
PubMed2003

Calcium signalling in and around the nuclear envelope.

We have compared calcium mobilization by Ins(1,4,5) P(3)(IP(3)), cADP-ribose (cADPR) and nicotinic acid-adenosine dinucleotide phosphate (NAADP) from the envelope of isolated nuclei with the calcium signalling in intact isolated pancreatic acinar cells. Ca(2+) uptake and release were studied with calcium-sensitive fluorescent probes. In the present study, we have shown that all calcium messengers induce Ca(2+) release from the nuclear envelope. Pre-treatment of nuclei with thapsigargin completely abolished the responses to the calcium messengers, indicating that Ca(2+) stores in isolated nuclei are thapsigargin-sensitive. Using different pharmacological tools, we show that Ca(2+) release from pancreatic nuclei is unlikely to occur from stores other than those with endoplasmic reticulum characteristics. We conclude that all three calcium messengers can release Ca(2+) from pancreatic acinar nuclear stores, as previously shown for IP(3) and cADPR. It would appear that NAADP releases Ca(2+) from the same IP(3)- and cADPR-sensitive stores with endoplasmic reticulum characteristics.

Animals↗
PubMed2005

Bimatoprost and prostaglandin F(2 alpha) selectively stimulate intracellular calcium signaling in different cat iris sphincter cells.

Bimatoprost is a synthetic analog of prostaglandin F(2 alpha) ethanolamide (prostamide F(2 alpha)), and shares a pharmacological profile consistent with that of the prostamides. Like prostaglandin F(2 alpha) carboxylic acid, bimatoprost potently lowers intraocular pressure in dogs, primates and humans. In order to distinguish its mechanism of action from prostaglandin F(2 alpha), fluorescence confocal microscopy was used to examine the effects of bimatoprost, prostaglandin F(2 alpha) and 17-phenyl prostaglandin F(2 alpha) on calcium signaling in resident cells of digested cat iris sphincter, a tissue which exhibits contractile responses to both agonists. Constant superfusion conditions obviated effective conversion of bimatoprost. Serial challenge with 100 nM bimatoprost and prostaglandin F(2 alpha) consistently evoked responses in different cells within the same tissue preparation, whereas prostaglandin F(2 alpha) and 17-phenyl prostaglandin F(2 alpha) elicited signaling responses in the same cells. Bimatoprost-sensitive cells were consistently re-stimulated with bimatoprost only, and prostaglandin F(2 alpha) sensitive cells could only be re-stimulated with prostaglandin F(2 alpha). The selective stimulation of different cells in the same cat iris sphincter preparation by bimatoprost and prostaglandin F(2 alpha), along with the complete absence of observed instances in which the same cells respond to both agonists, strongly suggests the involvement of distinct receptors for prostaglandin F(2 alpha) and bimatoprost. Further, prostaglandin F(2 alpha) but not bimatoprost potently stimulated calcium signaling in isolated human embryonic kidney cells stably transfected with the feline- and human-prostaglandin F(2 alpha) FP-receptor and in human dermal fibroblast cells, and only prostaglandin F(2 alpha) competed with radioligand binding in HEK-feFP cells. These studies provide further evidence for the existence of a bimatoprost-sensitive receptor that is distinct from any of the known prostaglandin receptor types.

Amides↗
PubMed2003

Fluid flow induced PGE2 release by bone cells is reduced by glycocalyx degradation whereas calcium signals are not.

It has been hypothesized that bone cells have a hyaluronic acid (HA) rich glycocalyx (cell coat or pericellular matrix) and that this contributes to bone cell mechanotransduction via fluid flow. The glycocalyx of bone cells of the MC3T3-E1 osteoblastic cell line and the MLO-Y4 osteocytic cell line were characterized. Alcian blue staining and lectin binding experiments suggested that these cells have a glycocalyx rich in HA. Sulphated proteoglycans were not detected. Staining with hyaluronic acid binding protein and degradation by hyaluronidase confirmed that HA was a major component of the glycocalyx. We subjected cells, with and without hyaluronidase treatment, to oscillating fluid flow under standardized in vitro conditions. There was no effect of glycocalyx degradation on the intracellular calcium signal, in either cell type, in terms of the percentage of cells responding (40-80%) or the magnitude of the response (2-5 times baseline). However, a 4-fold fluid flow induced increase in PGE2 was eliminated by hyaluronidase pre-treatment in MLO-Y4 cells. We conclude that under these conditions the calcium and PGE2 responses occur via different pathways. An intact glycocalyx is not necessary in order to initiate a calcium signal in response to oscillating fluid flow. However, in osteocyte-like cells the PGE2 pathway is more dependent on mechanical signals transmitted through the glycocalyx.

Animals↗
PubMed2002

HIV-1 Nef interacts with inositol trisphosphate receptor to activate calcium signaling in T cells.

HIV-1 pathogenicity factor Nef has been shown to modulate calcium signaling in host cells, but the underlying molecular mechanisms have remained unclear. Here we show that calcium/calcineurin-dependent activation of nuclear factor of activated T cells (NFAT) by Nef in Jurkat T cells requires the endoplasmic reticulum-resident inositol trisphosphate receptor (IP(3)R), but yet does not involve increase in phospholipase-C gamma 1 (PLC gamma 1)-catalyzed production of IP(3) or depletion of IP(3)-regulated intracellular calcium stores. Nef could be coprecipitated with endogenous IP(3)R type-1 (IP(3)R1) from Nef-transfected Jurkat T cells as well as from HIV-infected primary human peripheral mononuclear cells. Thus, the Nef/IP(3)R1-interaction defines a novel T cell receptor-independent mechanism by which Nef can promote T cell activation, and appears to involve atypical IP(3)R-triggered activation of plasma membrane calcium influx channels in a manner that is uncoupled from depletion of intracellular calcium stores.

Active Transport, Cell Nucleus↗
PubMed2001

Alterations in intracellular calcium signaling of lymphocytes after exhaustive exercise.

PURPOSE: Exhaustive exercise is accompanied by pronounced quantitative changes in leukocytes. Whereas most studies on lymphocytes have concentrated on their proliferative responses or cytokine secretion, not much is known about exercise-induced changes in intracellular signal transduction processes. In lymphocytes, the concentration of intracellular free calcium ([Ca(2+)](i)) is an important intracellular second messenger linking extracellular stimuli to cellular responses. The aim of the present study was to examine the effect of exhaustive exercise on the calcium homeostasis of lymphocytes. METHODS: Healthy volunteers underwent treadmill exercise at 80% of their maximal oxygen uptake until exhaustion. Blood samples were taken before, immediately after, 1 h after, and 1 d after the test. Lymphocyte subsets were analyzed by flow cytometry; isolation of lymphocytes was performed by density gradient centrifugation. [Ca(2+)](i) was measured using the calcium-sensitive fluorescent dye Fura-2. RESULTS: Compared with preexercise conditions, basal [Ca(2+)](i) was increased immediately after exercise, whereas there was no change after 1 h or 1 d. The anti-CD3- and phytohemagglutinin-induced Ca(2+) responses demonstrated a bivalent pattern. Immediately after exercise, Ca(2+) transients were impaired, whereas 1 h after and 1 d after the test, the Ca(2+) responses were increased. In contrast, the Ca(2+) responses induced by thapsigargin were not different at any time interval. Lymphocyte subsets increased immediately after exercise, especially natural killer cells and CD8+ T cells, and decreased below preexercise levels after 1 h. One day after exercise, cell counts were not different from preexercise levels. CONCLUSIONS: Taken together, this novel approach demonstrates that exhaustive exercise has a profound influence on intracellular calcium signaling of lymphocytes. These effects may explain changes in lymphocyte function that have previously been reported.

Adult↗
PubMed2001

[Mechanisms of generating calcium signals in exocrine acinar cells].

Review. Modern data about mechanisms of generation of the calcium signals in the exocrine acinar cells are presented. The mechanisms of inositol-1,4,5-trisphosphate- and Ca(2+)-induced Ca2+ release from intracellular stores of the acinar cells and mechanisms their influx from extracellular medium are described. The mechanisms which initiate Ca2+ oscillations and their role in the secretion of the fluid and enzymes by acinar cells are discussed.

Animals↗
PubMed2003

Ins(1,4,5)P3-mediated calcium signals and apoptosis: is there a role for Bcl-2?

In this review we speculate that the anti-apoptotic protein Bcl-2 may regulate calcium signals involved in mediating cell death. Evidence that Ins(1,4,5)P(3)-mediated calcium release from the endoplasmic reticulum triggers apoptosis in response to diverse signals is summarized. Also, we review evidence that Bcl-2 regulates calcium release from the endoplasmic reticulum, and speculate that Bcl-2 may interact either functionally or physically with Ins(1,4,5)P(3) receptors to modulate calcium signals that determine life or death decisions.

Animals↗
PubMed2006

Two system-size-resonance behaviors for calcium signaling: for optimal cell size and for optimal network size.

We have studied the collective calcium signaling behavior of an array of coupled N cells, taking into account the internal noises resulting from the small cell size V. The system's performance was characterized by the reciprocal coefficient of variance (RCV) of the calcium spike train. Two system-size resonances were observed, namely, the RCV value shows a clear peak when both N and V are optimal. Therefore, an optimal number of cells of optimal size work the best as a whole.

Animals↗
PubMed2003

Effects of beta-adrenergic blockers on glutamate-induced calcium signals in adult mouse retinal ganglion cells.

Betaxolol, a selective beta(1)-adrenoceptor antagonist, is an antiglaucoma drug commonly used to lower the intraocular pressure (IOP) in treatment of glaucoma. Recent evidence has also shown that it attenuates ligand- and voltage-gated currents in retinal ganglion cells, which may lead to reduction of intracellular calcium and prevention of glutamate-induced ganglion cell damage in glaucoma. In the present study, we examined the effectiveness of betaxolol and other beta-adrenergic blockers on glutamate-induced calcium signals. Dissociated adult mouse retinal ganglion cells were immuno-labeled with antibody CD90.2 and loaded with Fura-2AM. Calcium signals were recorded with optical recording techniques. Low doses of glutamate cause an increase in intracellular calcium that may result in pathological changes in ganglion cells. The action of glutamate could be reversibly suppressed by beta-adrenergic blockers and the order of inhibitory potency is (s)(-)-propranolol>betaxolol>>timolol, with average IC(50) of 78.05, 235.7 and 2167.05, microM, respectively. Betaxolol compressed the dose-response curve of glutamate. The EC(50) of glutamate was shifted from 6.19 to 23.53 microM, indicating that betaxolol acts as a non-competitive inhibitor of glutamate response in retinal ganglion cells. Our data are consistent with previous reports that betaxolol and other beta-adrenergic blockers may exert its neuroprotective action by suppression of glutamate-induced intracellular calcium increase in retinal ganglion cells.

Adrenergic beta-Agonists↗
PubMed2005

A three-dimensional model of intercellular calcium signaling in epithelial cells.

We have developed a fully three-dimensional (3D) model of calcium signaling in epithelial cells based on a set of reaction diffusion equations that are solved on a large-scale finite-element code in three dimensions. We have explicitly included the cellular compartments including the cell nucleus, cytoplasm, and gap junctions. The model allows for buffering of free Ca2+, calcium-induced calcium release, and the explicit inclusion of mobile buffers. To make quantitative comparisons to experimental results, we used fluorescence microscopy images of cells to generate an accurate mesh describing cell morphology. We found that Ca2+ wave propagation through the tissue is a function of both initial conditions used to start the wave and various geometrical parameters that affect propagation such as gap junction density and distribution, and the presence of nuclei. The exogenous dyes used in experimental imaging also affect wave propagation.

Animals↗
PubMed2005

Aberrant intracellular calcium signaling in olfactory neurons from patients with bipolar disorder.

OBJECTIVE: The authors examined the feasibility of using olfactory receptor neurons from living patients to test whether calcium signaling is altered in a neuronal cell population in bipolar disorder. METHOD: Ratiometric fluorescence photomicroscopy was used to assess basal and stimulus-induced changes in intracellular calcium levels in biopsy-derived olfactory receptor neurons from seven euthymic patients with bipolar disorder who were medication-free, 10 euthymic patients with bipolar disorder who were treated with mood stabilizers, and 17 age- and sex-matched comparison subjects without bipolar disorder. RESULTS: Olfactory receptor neurons from the seven medication-free patients responded to stimuli predominantly with decreases in intracellular calcium, unlike those from the seven matched healthy subjects. Olfactory receptor neurons from patients treated with mood stabilizers were less likely to respond to stimulation than olfactory receptor neurons from medication-free patients. CONCLUSIONS: This study demonstrates the feasibility of using olfactory receptor neurons to examine alterations in intracellular signaling in neuronal cells from living patients. Our results, although based on a small number of subjects, suggest that altered intracellular calcium signaling in olfactory receptor neurons may be a trait of bipolar disorder.

Anticonvulsants↗
PubMed2000

Meningeal cells can communicate with astrocytes by calcium signaling.

Mechanical stimulation of adult human and rat pia-arachnoid cell cultures (loaded with calcium indicator dye) produced an increase in calcium in the stimulated cell. This change then propagated rapidly among neighboring cells, producing a calcium wave with a maximum distance of propagation and velocity resembling calcium waves in astrocytes. The pia-arachnoid waves were blocked by either octanol or apyrase, suggesting that propagation might occur either by gap junction communication or extracellular movement of ATP. Calcium waves in pia-arachnoid cells could invade contiguous astrocytes, and vice versa. Gap junction coupling between pia-arachnoid cells and astrocytes was shown by dye transfer experiments, in conjunction with immunostaining for connexin43. We infer that calcium signals from cells in the cortical parenchyma may be transmitted to the pia-arachnoid and might then serve in the induction of neurovascular changes, including those postulated to be responsible for the pain of migraine headache.

Astrocytes↗
PubMed2004

Protease-activated receptor-1-induced calcium signaling in gingival fibroblasts is mediated by sarcoplasmic reticulum calcium release and extracellular calcium influx.

Thrombin is a serine protease activated during injury and inflammation. Thrombin and other proteases generated by periodontal pathogens affect the behavior of periodontal cells via activation of protease-activated receptors (PARs). We noted that thrombin and PAR-1 agonist peptide stimulated intracellular calcium levels ([Ca2+]i) of gingival fibroblasts (GF). This increase of [Ca2+]i was inhibited by EGTA and verapamil. U73122 and neomycin inhibited thrombin- and PAR-1-induced [Ca2+]i. Furthermore, 2-APB (75-100 microM, inositol triphosphate [IP3] receptor antagonist), thapsigargin (1 microM), SKF-96365 (200 microM) and W7 (50 and 100 microM) also suppressed the PAR-1- and thrombin-induced [Ca2+]i. However, H7 (100, 200 microM) and ryanodine showed little effects. Blocking Ca2+ efflux from mitochondria by CGP37157 (50, 100 microM) inhibited both thrombin- and PAR-1-induced [Ca2+]i. Thrombin induced the IP3 production of GF within 30-seconds of exposure, which was inhibited by U73122. These results indicate that mitochondrial calcium efflux and calcium-calmodulin pathways are related to thrombin and PAR-1 induced [Ca2+]i in GF. Thrombin-induced [Ca2+]i of GF is mainly due to PAR-1 activation, extracellular calcium influx via L-type calcium channel, PLC activation, then IP3 binding to IP3 receptor in sarcoplasmic reticulum, which leads to intracellular calcium release and subsequently alters cell membrane capacitative calcium entry.

Boron Compounds↗
PubMed1999

CAMs and FGF cause a local submembrane calcium signal promoting axon outgrowth without a rise in bulk calcium concentration.

Binding of basic fibroblast growth factor (bFGF) and cell adhesion molecules to the nerve cell membrane promotes axon outgrowth. This response can be blocked by antagonists of voltage-gated calcium channels, yet no change of cytosolic calcium concentration in the growth cone can be detected upon binding of the growth factor bFGF or the cell adhesion molecule L1. Using barium as a charge carrier, we show that bFGF and L1 open a calcium influx pathway in growth cones of rat sensory neurons without changing the membrane voltage. L1 does not activate influx in cells expressing a dominant negative mutant of the fibroblast growth factor receptor (FGFR) tyrosine kinase. FGFR-activated influx is blocked by specific antagonists of L- and N-type voltage-gated calcium channels and by an inhibitor of diacylglycerol lipase. We propose that both L1 and bFGF act via the FGFR to generate polyunsaturated fatty acids which in turn cause calcium channels to flicker open and shut. Short-lived domains of raised calcium at the cytosolic mouth of open channels activate axon outgrowth without raising bulk cytosolic calcium concentration. In confirmation of this model, the rapidly-acting calcium buffer BAPTA is significantly more effective at blocking FGF-induced axon outgrowth when compared with the slower buffer EGTA. Generation of short-lived calcium domains may provide a crucial mechanism for axon guidance during development and for promoting regeneration of damaged axons.

Animals↗
PubMed1999

Protein targeting and calcium signaling microdomains in neuronal cells.

Over the last several years, a number of optical imaging, physiological, and molecular studies have clarified the mechanisms underlying differential calcium signaling in the postsynaptic neuron. These studies have revealed the existence of membrane-associated calcium microdomains, which are often specifically coupled to distinct protein signaling pathways. In this review, we discuss how these signaling microdomains are organized and regulated, emphasizing the structural and molecular features of synaptic protein complexes containing the metabotropic and N-methyl-D-aspartate (NMDA) glutamate receptors and the L-type voltage-dependent calcium channels (VDCCs). We conclude with a discussion of how these different signaling complexes may interact with one another, relationships which may be important in orchestrating the complex calcium signaling underlying developmental and activity-dependent changes in synaptic function.

Animals↗
PubMed1997

Calcium signalling in the cell nucleus.

The First European Conference on Calcium Signalling in the Cell Nucleus took place in Baia Paraelios, Calabria, Italy, from 4-8 October 1997. It was organized by O. Bachs, E. Carafoli, P. Nicotera and L. Santella (local organizers, G. Bagetta and D. Rotiroti) and attended by about 90 specialists. The scientific content was very high and the discussions were particularly intense. Considering that the area is famous for its controversies, one could perhaps have expected aggressive overtones. Instead, in spite of the liveliness of the discussions, the atmosphere was congenial and constructive. The controversies have not disappeared, but a better understanding of some of their origins is now well under way.

Calcium↗
PubMed1988

Interaction of atrial natriuretic peptide-stimulated guanylate cyclase and vasopressin-stimulated calcium signaling pathways in the glomerular mesangial cell.

Receptors for atrial natriuretic peptide (ANP) have been demonstrated in renal mesangial cells as well as other cell types in the glomerulus. The biochemical basis for the effects of ANP on glomerular hemodynamics remains undefined. Using cultured rat glomerular mesangial cells, we demonstrated a concentration-dependent stimulation of cGMP production in intact cells, and of guanylate cyclase in membranes. Despite the presence of a guanylate cyclase response, ANP had no inhibitory effect on basal inositol trisphosphate production nor on basal cytosolic calcium. Arginine vasopressin stimulated IP3 production, caused a rise in cytosolic calcium as measured using the calcium-sensitive fluorescent probe Indo-1, and caused mesangial cell contraction. ANP caused a slight but significant enhancement of vasopressin-stimulated IP3 production, but had no effect on the cytosolic calcium response nor on the contractile response. 8-Bromo-cGMP likewise had no effect on the generation of the calcium signal. These results indicate that the effects of ANP on glomerular hemodynamics are not mediated by an alteration in the generation of the calcium signal in mesangial cells. In contrast, addition of calcium inhibited ANP stimulated guanylate cyclase activity.

1-Methyl-3-isobutylxanthine↗
PubMed1986

Loss of secretory response of rat basophilic leukemia (2H3) cells at 40 degrees C is associated with reversible suppression of inositol phospholipid breakdown and calcium signals.

Antigen-induced stimulatory signals as well as histamine secretion from the RBL-2H3 cells were found to be highly temperature dependent. There was no hydrolysis of inositol phospholipids, increase in cytosol calcium concentration (calcium signal), or secretion upon antigen stimulation at temperatures below 20 degrees C. At higher temperatures (i.e., 20 to 37 degrees C), all responses increased in extent with increase in temperature. Temperatures of 38 degrees C or higher, however, resulted in a marked decline in all responses, until no responses were observed at 40 to 42 degrees C. As indicated by the decay in calcium signal, the duration of response was also temperature dependent. The response was of long duration at 30 to 32 degrees C, but it became progressively more transient as the temperature was increased from 32 to 40 degrees C. The effects of low or high temperature were fully reversible. For example, in the presence of antigen, stimulatory signals immediately appeared once the temperature was decreased from 40 to 37 degrees C. Although the diminished responses could be explained, in part, by a reduction in rates of IgE receptor aggregation and phospholipase C activity, the reductions were insufficient to account for complete loss of activity at 40 degrees C. We conclude that generation of intracellular signals in 2H3 cells is blocked by quite small elevations in temperature above 37 degrees C, possibly as consequence of changes in membrane fluidity.

Animals↗