Effect of piracetam on polyphosphoinositide metabolism, cytosolic calcium release, and oxidative burst in human polymorphonuclear cells: interaction with fMLP-induced stimulation

1999 ◽  
Vol 57 (2) ◽  
pp. 163-170 ◽  
Author(s):  
Michèle Tissot ◽  
Gilles Sarfati ◽  
Monique Roch-Arveiller ◽  
Jean-Paul Giroud
Keyword(s):  
Oxidative Burst ◽  
Calcium Release ◽  
Cytosolic Calcium ◽  
Polymorphonuclear Cells ◽  
Polyphosphoinositide Metabolism

scholarly journals Orientia tsutsugamushi Inhibits Apoptosis of Macrophages by Retarding Intracellular Calcium Release

2002 ◽  
Vol 70 (8) ◽  
pp. 4692-4696 ◽  
Author(s):  
Mee-Kyung Kim ◽  
Seung-Yong Seong ◽  
Ju-Young Seoh ◽  
Tae-Hee Han ◽  
Hyeon-Je Song ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Release ◽  
Cytosolic Calcium ◽  
Orientia Tsutsugamushi ◽  
Cytosolic Calcium Concentration ◽  
Infected Cells ◽  
Intracellular Calcium Release ◽  
Calcium Redistribution ◽  
In Cells

ABSTRACT Orientia tsutsugamushi shows both pro- and antiapoptotic activities in infected vertebrate cells. Apoptosis of THP-1 cells induced by beauvericin was inhibited by O. tsutsugamushi infection. Beauvericin-induced calcium redistribution was significantly reduced and retarded in cells infected with O. tsutsugamushi. Antiapoptotic activities of O. tsutsugamushi in infected cells are most probably due to inhibition of the increase in the cytosolic calcium concentration.

scholarly journals Injection of inositol trisphosphorothioate into Limulus ventral photoreceptors causes oscillations of free cytosolic calcium.

1991 ◽  
Vol 97 (6) ◽  
pp. 1165-1186 ◽  
Author(s):  
R Payne ◽  
B V Potter
Keyword(s):  
Membrane Potential ◽  
Calcium Release ◽  
Feedback Inhibition ◽  
Initial Response ◽  
Periodic Variation ◽  
Cytosolic Calcium ◽  
Ion Concentration ◽  
Free Calcium ◽  
Calcium Stores ◽  
Calcium Ion Concentration

Limulus ventral photoreceptors contain calcium stores sensitive to release by D-myo-inositol 1,4,5 trisphosphate (InsP3) and a calcium-activated conductance that depolarizes the cell. Mechanisms that terminate the response to InsP3 were investigated using nonmetabolizable DL-myo-inositol 1,4,5 trisphosphorothioate (InsPS3). An injection of 1 mM InsPS3 into a photoreceptor's light-sensitive lobe caused an initial elevation of cytosolic free calcium ion concentration (Cai) and a depolarization lasting only 1-2 s. A period of densensitization followed, during which injections of InsPS3 were ineffective. As sensitivity recovered, oscillations of membrane potential began, continuing for many minutes with a frequency of 0.07-0.3 Hz. The activity of InsPS3 probably results from the D-stereoisomer, since L-InsP3 was much less effective than InsP3. Injections of 1 mM InsP3 caused an initial depolarization and a period of densensitization similar to that caused by 1 mM InsPS3, but no sustained oscillations of membrane potential. The initial response to InsPS3 or InsP3 may therefore be terminated by densensitization, rather than by metabolism. Metabolism of InsP3 may prevent oscillations of membrane potential after sensitivity has recovered. The InsPS3-induced oscillations of membrane potential accompanied oscillations of Cai and were abolished by injection of ethyleneglycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid. Removal of extracellular calcium reduced the frequency of oscillation but not its amplitude. Under voltage clamp, oscillations of inward current were observed. These results indicate that periodic bursts of calcium release underly the oscillations of membrane potential. After each burst, the sensitivity of the cell to injected InsP3 was greatly reduced, recovering during the interburst interval. The oscillations may, therefore, result in part from a periodic variation in sensitivity to a constant concentration of InsPS3. Prior injection of calcium inhibited depolarization by InsPS3, suggesting that feedback inhibition of InsPS3-induced calcium release by elevated Cai may mediate desensitization between bursts and after injections of InsPS3.

ATP induces contraction of cultured brain capillary pericytes, via activation of P2Y type purinergic receptors

2020 ◽  
Author(s):  
Sofie Hørlyck ◽  
Changsi Cai ◽  
Hans C Helms ◽  
Martin Lauritzen ◽  
Birger Brodin
Keyword(s):  
Intracellular Calcium ◽  
Purinergic Receptors ◽  
Calcium Release ◽  
Purinergic Receptor ◽  
Cytosolic Calcium ◽  
Receptor Activation ◽  
Confocal Imaging ◽  
Inositol Triphosphate ◽  
Brain Capillary

Brain capillary pericytes have been suggested to play a role in the regulation of cerebral blood-flow under physiological and pathophysiological conditions. ATP has been shown to cause constriction of capillaries under ischemic conditions and suggested to be involved in the "no-reflow" phenomenon. In order to investigate the effects of extracellular ATP on pericyte cell contraction, we studied purinergic receptor activation of cultured bovine brain capillary pericytes. We measured [Ca2+]i-responses to purinergic agonists with the fluorescent indicators fura-2 and Cal-520 and estimated contraction of pericytes as relative change in cell area, using real-time confocal imaging. Addition of ATP caused an increase in cytosolic calcium and contraction of the brain capillary pericytes, both reversible and inhibited by a purinergic receptor antagonist PPADS. Furthermore, we demonstrated that ATP-induced contraction could be eliminated by intracellular calcium-chelation with BAPTA, indicating that the contraction was mediated via purinergic P2 -type receptor-mediated [Ca2+]i-signaling. ATP stimulation induced inositol triphosphate signaling, consistent with the notion of P2Y receptor activation. Receptor profiling studies demonstrated presence of P2Y1 and P2Y2 receptors, using ATP, UTP, ADP and the subtype specific agonists MRS2365 (P2Y1) and 2-thio-UTP (P2Y2)). Addition of specific P2X agonists only caused a [Ca2+]i increase at high concentrations, attributed to activation of inositol triphosphate signaling. Our results suggest that contraction of brain capillary pericytes in vitro by activation of P2Y type purinergic receptors is caused by intracellular calcium release. This adds more mechanistic understanding to the role of pericytes in vessel constriction, and points towards P2Y receptors as potential therapeutic targets.

Mechanism of phorbol ester inhibition of histamine-induced IP3 formation in cultured airway smooth muscle

1989 ◽  
Vol 257 (4) ◽  
pp. L209-L216 ◽  
Author(s):  
R. K. Murray ◽  
C. F. Bennett ◽  
S. J. Fluharty ◽  
M. I. Kotlikoff
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Calcium Release ◽  
Calcium Sensitivity ◽  
Cytosolic Calcium ◽  
Guanine Nucleotide ◽  
Intact Cells ◽  
Kinase C ◽  
Inositol 1,4,5 Trisphosphate ◽  
Site Of Action

Cytosolic calcium is a key determinant of the contractile state of airway smooth muscle (ASM). To investigate the mechanisms by which histamine affects cytosolic calcium, we measured changes in inositol 1,4,5-trisphosphate (IP3) following the addition of histamine to cultured canine ASM cells. The effect of phorbol 12-myristate 13-acetate (PMA) on IP3 formation was investigated under conditions previously shown to abolish histamine-induced calcium release. In both intact cells and ASM membranes, histamine produced a significant increase in IP3 formation, which was inhibited by PMA. The site of this blockade was investigated by examining the effect of PMA on guanine nucleotide-stimulated IP3 formation and on phosphoinositide-specific phospholipase C (PI-PLC) activity in ASM membranes. Guanine nucleotide-stimulated IP3 formation was inhibited by PMA pretreatment. Membrane-associated PI-PLC activity was also decreased, an effect that was not due simply to a shift in the calcium sensitivity of the enzyme. We conclude that in cultured canine ASM cells, PMA blocks histamine-induced IP3 formation and that this inhibition is caused, in part, by a postreceptor site of action of protein kinase C, possibly via a direct effect on PI-PLC.

scholarly journals Sodium/Calcium Exchangers Selectively Regulate Calcium Signaling in Mouse Taste Receptor Cells

2010 ◽  
Vol 104 (1) ◽  
pp. 529-538 ◽  
Author(s):  
Steven A. Szebenyi ◽  
Agnieszka I. Laskowski ◽  
Kathryn F. Medler
Keyword(s):  
Calcium Release ◽  
Calcium Influx ◽  
Taste Receptor ◽  
Physiological Role ◽  
Cytosolic Calcium ◽  
Calcium Signals ◽  
Sodium Calcium ◽  
Signaling Mechanisms ◽  
Taste Cells ◽  
Mouse Taste

Taste cells use multiple signaling mechanisms to generate appropriate cellular responses to discrete taste stimuli. Some taste stimuli activate G protein coupled receptors (GPCRs) that cause calcium release from intracellular stores while other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). While the signaling mechanisms that initiate calcium signals have been described in taste cells, the calcium clearance mechanisms (CCMs) that contribute to the termination of these signals have not been identified. In this study, we used calcium imaging to define the role of sodium-calcium exchangers (NCXs) in the termination of evoked calcium responses. We found that NCXs regulate the calcium signals that rely on calcium influx at the plasma membrane but do not significantly contribute to the calcium signals that depend on calcium release from internal stores. Our data indicate that this selective regulation of calcium signals by NCXs is due primarily to their location in the cell rather than to the differences in cytosolic calcium loads. This is the first report to define the physiological role for any of the CCMs utilized by taste cells to regulate their evoked calcium responses.

scholarly journals Control of the Oxidative Burst of Human Neutrophils by Staphylococcal Leukotoxins

2003 ◽  
Vol 71 (7) ◽  
pp. 3724-3729 ◽  
Author(s):  
Didier A. Colin ◽  
Henri Monteil
Keyword(s):  
Flow Cytometry ◽  
Oxidative Burst ◽  
Pore Formation ◽  
Human Neutrophils ◽  
Polymorphonuclear Cells ◽  
Phosphatidylinositol 3 Kinase ◽  
Intracellular Release ◽  
Two Component ◽  
Phosphatidylinositol 3

ABSTRACT The ability of staphylococcal two-component leukotoxins to induce an oxidative burst and/or to prime human polymorphonuclear cells (PMNs) was studied by using spectrofluorometry or flow cytometry. At sublytic concentrations, the HlgA-HlgB, HlgA-LukF-PV, LukS-PV-LukF-PV, and HlgC-LukF-PV combinations of leukotoxins, but not the LukS-PV-HlgB and HlgC-HlgB combinations, were able to induce H2O2 production similar to the H2O2 production induced by 1 μM N-formyl-Met-Leu-Phe (fMLP). In addition, when added at sublytic concentrations, all of the leukotoxin combinations primed PMNs for H2O2 production induced by fMLP. Leukotoxin activation was dependent on the presence of Ca2+ and was inhibited by wortmannin, an inhibitor of phosphatidylinositol 3-kinase, but not by N-methyl-l-arginine, an inhibitor of NO generation, which eliminates the possibility that NO plays a role in the action of leukotoxins. At higher concentrations, all leukotoxins inhibited H2O2 production by PMNs activated by fMLP, phorbol 12-myristate 13-acetate (PMA), or the leukotoxins themselves. This inhibition was not related to the pore formation induced by leukotoxins. Intracellular release of H2O2 induced by fMLP and PMA was not primed by leukotoxins but was inhibited. It seems that leukotoxin inhibition of H2O2 release is independent of pore formation but secondary to an intracellular event, as yet unknown, triggered by leukotoxins.

scholarly journals Calcium-Induced Calcium Release in Smooth Muscle

2000 ◽  
Vol 115 (5) ◽  
pp. 653-662 ◽  
Author(s):  
M.L. Collier ◽  
G. Ji ◽  
Y.-X. Wang ◽  
M.I. Kotlikoff
Keyword(s):  
Smooth Muscle ◽  
Calcium Release ◽  
Striated Muscle ◽  
Single Channel ◽  
Ryanodine Receptors ◽  
Cytosolic Calcium ◽  
Heart Cells ◽  
Tight Coupling ◽  
Calcium Induced Calcium Release ◽  
Ca2 Channels

Calcium-induced calcium release (CICR) has been observed in cardiac myocytes as elementary calcium release events (calcium sparks) associated with the opening of L-type Ca2+ channels. In heart cells, a tight coupling between the gating of single L-type Ca2+ channels and ryanodine receptors (RYRs) underlies calcium release. Here we demonstrate that L-type Ca2+ channels activate RYRs to produce CICR in smooth muscle cells in the form of Ca2+ sparks and propagated Ca2+ waves. However, unlike CICR in cardiac muscle, RYR channel opening is not tightly linked to the gating of L-type Ca2+ channels. L-type Ca2+ channels can open without triggering Ca2+ sparks and triggered Ca2+ sparks are often observed after channel closure. CICR is a function of the net flux of Ca2+ ions into the cytosol, rather than the single channel amplitude of L-type Ca2+ channels. Moreover, unlike CICR in striated muscle, calcium release is completely eliminated by cytosolic calcium buffering. Thus, L-type Ca2+ channels are loosely coupled to RYR through an increase in global [Ca2+] due to an increase in the effective distance between L-type Ca2+ channels and RYR, resulting in an uncoupling of the obligate relationship that exists in striated muscle between the action potential and calcium release.

scholarly journals Reperfusion after Ichemia Causes Cytosolic Calcium Overload Due to Rapid Calcium Release from the Sarcoplasmic Reticulum

2009 ◽  
Vol 96 (3) ◽  
pp. 550a
Author(s):  
Carlos A. Valverde ◽  
Dmytro Kornyeyev ◽  
Alicia R. Mattiazzi ◽  
Ariel L. Escobar
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Cytosolic Calcium ◽  
Calcium Overload
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