Journal articles on the topic 'ATP Wave'
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1
Sauer, H., J. Hescheler, and M. Wartenberg. "Mechanical strain-induced Ca2+waves are propagated via ATP release and purinergic receptor activation." American Journal of Physiology-Cell Physiology 279, no. 2 (August 1, 2000): C295—C307. http://dx.doi.org/10.1152/ajpcell.2000.279.2.c295.
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Mechanical strain applied to prostate cancer cells induced an intracellular Ca2+ (Cai 2+) wave spreading with a velocity of 15 μm/s. Cai 2+ waves were not dependent on extracellular Ca2+ and membrane potential because propagation was unaffected in high-K+ and Ca2+-free solution. Waves did not depend on the cytoskeleton or gap junctions because cytochalasin B and nocodazole, which disrupt microfilaments and microtubules, respectively, and 1-heptanol, which uncouples gap junctions, were without effects. Fluorescence recovery after photobleaching experiments revealed an absence of gap junctional coupling. Cai 2+ waves were inhibited by the purinergic receptor antagonists basilen blue and suramin; by pretreatment with ATP, UTP, ADP, UDP, 2-methylthio-ATP, and benzoylbenzoyl-ATP; after depletion of ATP by 2-deoxyglucose; and after ATP scavenging by apyrase. Waves were abolished by the anion channel inhibitors 5-nitro-2-(3-phenylpropylamino)benzoic acid, tamoxifen, 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid, niflumic acid, and gadolinium. ATP release following strain was significantly inhibited by anion channel blockers. Hence, ATP is secreted via mechanosensitive anion channels and activates purinergic receptors on the same cell or neighboring cells in an autocrine and paracrine manner, thus leading to Cai 2+ wave propagation.
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Bowser, David N., and Baljit S. Khakh. "Vesicular ATP Is the Predominant Cause of Intercellular Calcium Waves in Astrocytes." Journal of General Physiology 129, no. 6 (May 15, 2007): 485–91. http://dx.doi.org/10.1085/jgp.200709780.
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Brain astrocytes signal to each other and neurons. They use changes in their intracellular calcium levels to trigger release of transmitters into the extracellular space. These can then activate receptors on other nearby astrocytes and trigger a propagated calcium wave that can travel several hundred micrometers over a timescale of seconds. A role for endogenous ATP in calcium wave propagation in hippocampal astrocytes has been suggested, but the mechanisms remain incompletely understood. Here we explored how calcium waves arise and directly tested whether endogenously released ATP contributes to astrocyte calcium wave propagation in hippocampal astrocytes. We find that vesicular ATP is the major, if not the sole, determinant of astrocyte calcium wave propagation over distances between ∼100 and 250 μm, and ∼15 s from the point of wave initiation. These actions of ATP are mediated by P2Y1 receptors. In contrast, metabotropic glutamate receptors and gap junctions do not contribute significantly to calcium wave propagation. Our data suggest that endogenous extracellular astrocytic ATP can signal over broad spatiotemporal scales.
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Okamoto, KI, and Y. Nakaoka. "RECONSTITUTION OF METACHRONAL WAVES IN CILIATED CORTICAL SHEETS OF PARAMECIUM - WAVE STABILITIES." Journal of Experimental Biology 192, no. 1 (July 1, 1994): 61–72. http://dx.doi.org/10.1242/jeb.192.1.61.
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We reconstituted metachronal waves on ciliated cortical sheets prepared from detergent-extracted Paramecium multimicronucleatum cells. Ciliary movements of the cortical sheet, whose intracellular side adhered to a glass coverslip, were reactivated by perfusion of a basic reactivation medium containing ATP. In this condition, the ciliary field showed only unstable localised ripples. Addition of either cyclic AMP or cyclic GMP to the basic reactivation medium generated propagating metachronal waves characteristic of each nucleotide. In order to estimate the stability of the metachronal waves, autocorrelation coefficients were calculated from images of an 8 µm diameter region within the reactivated ciliary field. The decay time for the correlation coefficient to decrease to 0.5 was only 0.04 s in the basic reactivation medium, but was increased to 0.4 or 0.9 s by the addition of cyclic AMP or cyclic GMP, respectively. The decay time was dependent not only on the concentration of cyclic nucleotide but also on the wave frequency. In order to test whether cyclic-nucleotide-dependent phosphorylation affected the generation of waves, the ciliated cortical sheets were thiophosphorylated by incubation in ATP-gamma-S (adenosine-5'-o-3-thiotriphosphate) medium containing either cyclic AMP or cyclic GMP. Following this, perfusion with the basic reactivation medium generated metachronal waves only after cyclic GMP treatment. The effect of cyclic GMP is probably related to phosphorylation of ciliary proteins.
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Skorinkin, A. I., R. A. Giniatullin, and K. B. Ostroumov. "Modeling of two-wave ATP-induced currents." Neurophysiology 32, no. 3 (May 2000): 229. http://dx.doi.org/10.1007/bf02506590.
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Kim, Joon-Chul, Min-Jeong Son, and Sun-Hee Woo. "Ca2+ Signaling Triggered by Shear-Autocrine P2X Receptor Pathway in Rat Atrial Myocytes." Cellular Physiology and Biochemistry 50, no. 6 (2018): 2296–313. http://dx.doi.org/10.1159/000495089.
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Background/Aims: The atrium is exposed to high shear stress during heart failure and valvular diseases. We aimed to understand atrial shear-induced Ca2+ signaling and its underlying mechanisms. Methods: Pressurized micro-flow was applied to single rat atrial myocytes, and Ca2+ signal, membrane potential, and ATP release were assessed using confocal imaging, patch clamp technique, and luciferin-luciferase assay, respectively. Results: Shear stress (∼16 dyn/cm2) induced global Ca2+ waves (∼0.1 events/s) from the periphery to the center of cells in a transverse direction (“T-wave”; ∼145 μm/s). Pharmacological interventions and simultaneous recording of membrane potential and Ca2+ demonstrated that shear-induced T-waves resulted from action potential (AP)-triggered Ca2+ release from the sarcoplasmic reticulum. T-waves were not sensitive to inhibitors of known shear signaling mechanisms except connexin hemichannels and ATP release. Shear stress caused ATP release from these myocytes (∼1.1x10-17 moles/unit membrane, µm2); ATP release was increased by enhancement of connexin hemichannels and suppressed by inhibition of the hemichannels, but not affected by inhibitors of other ATP release pathways. Blockade of P2X receptor, but not pannexin or the Na+-Ca2+ exchanger, eliminated shear-induced T-wave initiation. Conclusion: Our data suggest that shear stress triggers APs and concomitant Ca2+ signaling via activation of P2X receptors by connexin hemichannel-mediated ATP release in atrial myocytes.
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Samuels, Stuart E., Jeffrey B. Lipitz, Gerhard Dahl, and Kenneth J. Muller. "Neuroglial ATP release through innexin channels controls microglial cell movement to a nerve injury." Journal of General Physiology 136, no. 4 (September 27, 2010): 425–42. http://dx.doi.org/10.1085/jgp.201010476.
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Microglia, the immune cells of the central nervous system, are attracted to sites of injury. The injury releases adenosine triphosphate (ATP) into the extracellular space, activating the microglia, but the full mechanism of release is not known. In glial cells, a family of physiologically regulated unpaired gap junction channels called innexons (invertebrates) or pannexons (vertebrates) located in the cell membrane is permeable to ATP. Innexons, but not pannexons, also pair to make gap junctions. Glial calcium waves, triggered by injury or mechanical stimulation, open pannexon/innexon channels and cause the release of ATP. It has been hypothesized that a glial calcium wave that triggers the release of ATP causes rapid microglial migration to distant lesions. In the present study in the leech, in which a single giant glial cell ensheathes each connective, hydrolysis of ATP with 10 U/ml apyrase or block of innexons with 10 µM carbenoxolone (CBX), which decreased injury-induced ATP release, reduced both movement of microglia and their accumulation at lesions. Directed movement and accumulation were restored in CBX by adding ATP, consistent with separate actions of ATP and nitric oxide, which is required for directed movement but does not activate glia. Injection of glia with innexin2 (Hminx2) RNAi inhibited release of carboxyfluorescein dye and microglial migration, whereas injection of innexin1 (Hminx1) RNAi did not when measured 2 days after injection, indicating that glial cells’ ATP release through innexons was required for microglial migration after nerve injury. Focal stimulation either mechanically or with ATP generated a calcium wave in the glial cell; injury caused a large, persistent intracellular calcium response. Neither the calcium wave nor the persistent response required ATP or its release. Thus, in the leech, innexin membrane channels releasing ATP from glia are required for migration and accumulation of microglia after nerve injury.
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Agladze, Konstantin, Matthew W. Kay, Valentin Krinsky, and Narine Sarvazyan. "Interaction between spiral and paced waves in cardiac tissue." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 1 (July 2007): H503—H513. http://dx.doi.org/10.1152/ajpheart.01060.2006.
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For prevention of lethal arrhythmias, patients at risk receive implantable cardioverter-defibrillators, which use high-frequency antitachycardia pacing (ATP) to convert tachycardias to a normal rhythm. One of the suggested ATP mechanisms involves paced-induced drift of rotating waves followed by their collision with the boundary of excitable tissue. This study provides direct experimental evidence of this mechanism. In monolayers of neonatal rat cardiomyocytes in which rotating waves of activity were initiated by premature stimuli, we used the Ca2+-sensitive indicator fluo 4 to observe propagating wave patterns. The interaction of the spiral tip with a paced wave was then monitored at a high spatial resolution. In the course of the experiments, we observed spiral wave pinning to local heterogeneities within the myocyte layer. High-frequency pacing led, in a majority of cases, to successful termination of spiral activity. Our data show that 1) stable spiral waves in cardiac monolayers tend to be pinned to local heterogeneities or areas of altered conduction, 2) overdrive pacing can shift a rotating wave from its original site, and 3) the wave break, formed as a result of interaction between the spiral tip and a paced wave front, moves by a paced-induced drift mechanism to an area where it may become unstable or collide with a boundary. The data were complemented by numerical simulations, which was used to further analyze experimentally observed behavior.
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Li, Yang, Lynne A. Holtzclaw, and James T. Russell. "Müller Cell Ca2+ Waves Evoked by Purinergic Receptor Agonists in Slices of Rat Retina." Journal of Neurophysiology 85, no. 2 (February 1, 2001): 986–94. http://dx.doi.org/10.1152/jn.2001.85.2.986.
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We have measured agonist evoked Ca2+ waves in Müller cells in situ within freshly isolated retinal slices. Using an eye cup dye loading procedure we were able to preferentially fill Müller glial cells in retinal slices with calcium green. Fluorescence microscopy revealed that bath perfusion of slices with purinergic agonists elicits Ca2+ waves in Müller cells, which propagate along their processes. These Ca2+ signals were insensitive to tetrodotoxin (TTX, 1.0 μM) pretreatment. Cells were readily identified as Müller cells by their unique morphology and by subsequent immunocytochemical labeling with glial fibrillary acidic protein antibodies. While cells never exhibited spontaneous Ca2+ oscillations, purinoreceptor agonists, ATP, 2 MeSATP, ADP, 2 MeSADP, and adenosine readily elicited Ca2+ waves. These waves persisted in the absence of [Ca2+]o but were abolished by thapsigargin pretreatment, suggesting that the purinergic agonists tested act by releasing Ca2+ from intracellular Ca2+ stores. The rank order of potency of different purines and pyrimidines for inducing Ca2+ signals was 2 MeSATP = 2MeSADP > ADP > ATP ≫ αβmeATP = uridine triphosphate (UTP) > uridine diphosphate (UDP). The Ca2+signals evoked by ATP, ADP, and 2 MeSATP were inhibited by reactive blue (100 μM) and suramin (200 μM), and the adenosine induced signals were abolished only by 3,7-dimethyl-1-propargylxanthine (200 μM) and not by 1,3-dipropyl-8-(2-amino-4-chlorophenyl)-xanthine) or 8-cyclopentyl-1,3-dipropylxanthine at the same concentration. Based on these pharmacological characteristics and the dose-response relationships for ATP, 2 MeSATP, 2 MeSADP, ADP, and adenosine, we concluded that Müller cells express the P1A2 and P2Y1 subtypes of purinoceptors. Analysis of Ca2+ responses showed that, similar to glial cells in culture, wave propagation occurred by regenerative amplification at specialized Ca2+ release sites (wave amplification sites), where the rate of Ca2+ release was significantly enhanced. These data suggest that Müller cells in the retina may participate in signaling, and this may serve as an extra-neuronal signaling pathway.
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Hansen, M., S. Boitano, E. R. Dirksen, and M. J. Sanderson. "Intercellular calcium signaling induced by extracellular adenosine 5′-triphosphate and mechanical stimulation in airway epithelial cells." Journal of Cell Science 106, no. 4 (December 1, 1993): 995–1004. http://dx.doi.org/10.1242/jcs.106.4.995.
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Airway epithelial cells in culture respond to extracellular adenosine 5′-triphosphate (ATP) by increasing their intracellular Ca2+ concentration ([Ca2+]i). The effective concentration of ATP that elicited a Ca2+ response equal to 50% of the maximal response (EC50) was 0.5 microM. Release of ATP from a pipette to form a local gradient of ATP increased [Ca2+]i of individual cells in a sequential manner. Cells closest to the pipette showed an immediate increase in [Ca2+]i while more distal cells displayed a delayed increase in [Ca2+]i. This response to the local release of ATP appeared as a wave of increasing [Ca2+]i that spread to several cells and, in this respect, was similar to the intercellularly communicated Ca2+ waves initiated by mechanical stimulation in airway epithelial cells (Sanderson et al., Cell Regul. 1, 585–596, 1990). In the presence of a unidirectional fluid flow, the Ca2+ response to a local release of ATP was biased such that virtually all the cells responding with an increase in [Ca2+]i were downstream of the release site. By contrast, an identical fluid flow did not bias the radial propagation of intercellular Ca2+ waves induced by mechanical stimulation. Suramin, a P2-purinergic receptor antagonist, did attenuate the Ca2+ response induced by ATP but did not block the propagation of mechanically induced Ca2+ waves. Cells from young cultures (3-5 days) or those at the leading edge of an outgrowth elevated their [Ca2+]i in response to ATP. However, these cells do not respond to mechanical stimulation by the propagation of a Ca2+ wave. From these results we conclude that the intercellular Ca2+ waves elicited by mechanical stimulation are not the result of ATP or another compound released from the stimulated cell, diffusing through the extracellular fluid. This conclusion is consistent with previous experimental evidence suggesting that intercellular Ca2+ signaling in epithelial cells is mediated by the movement of inositol trisphosphate through gap junctions.
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Lu, Jian Xu, and Cheng Jia Ma. "Research on Electrical Engineering with a New Fault Location Method of Double Terminal Based on HHT." Advanced Materials Research 1003 (July 2014): 124–29. http://dx.doi.org/10.4028/www.scientific.net/amr.1003.124.
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Among the available fault location methods based on traveling waves, calibrations of wave velocity and wave arrival time are the two main problems. This paper proposes a new fault location method which combines the two problems mentioned above. In this method, the first wave and second wave obtained at one side and the first wave obtained at the other side is used to locate the fault point. And the Hilbert-Huang transform is used in the calibration of wave arrival time, making the method more accurate than using wavelet transform. This method has the following two advantages: At first, it dismisses the influence of wave velocity. In the second, it doesn’t need to distinguish the sources of the received waves. ATP-EMTP’s simulation results show that this method is available and the location precision is higher than traditional fault location methods.
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Huo, Bo, Xin L. Lu, and X. Edward Guo. "Intercellular calcium wave propagation in linear and circuit-like bone cell networks." Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences 368, no. 1912 (February 13, 2010): 617–33. http://dx.doi.org/10.1098/rsta.2009.0221.
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In the present study, the mechanism of intercellular calcium wave propagation in bone cell networks was identified. By using micro-contact printing and self-assembled monolayer technologies, two types of in vitro bone cell networks were constructed: open-ended linear chains and looped hexagonal networks with precisely controlled intercellular distances. Intracellular calcium responses of the cells were recorded and analysed when a single cell in the network was mechanically stimulated by nano-indentation. The looped cell network was shown to be more efficient than the linear pattern in transferring calcium signals from cell to cell. This phenomenon was further examined by pathway-inhibition studies. Intercellular calcium wave propagation was significantly impeded when extracellular adenosine triphosphate (ATP) in the medium was hydrolysed. Chemical uncoupling of gap junctions, however, did not significantly decrease the transferred distance of the calcium wave in the cell networks. Thus, it is extracellular ATP diffusion, rather than molecular transport through gap junctions, that dominantly mediates the transmission of mechanically elicited intercellular calcium waves in bone cells. The inhibition studies also demonstrated that the mechanical stimulation-induced calcium responses required extracellular calcium influx, whereas the ATP-elicited calcium wave relied on calcium release from the calcium store of the endoplasmic reticulum.
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Handly, L. Naomi, and Roy Wollman. "Wound-induced Ca2+ wave propagates through a simple release and diffusion mechanism." Molecular Biology of the Cell 28, no. 11 (June 2017): 1457–66. http://dx.doi.org/10.1091/mbc.e16-10-0695.
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Damage-associated molecular patterns (DAMPs) are critical mediators of information concerning tissue damage from damaged cells to neighboring healthy cells. ATP acts as an effective DAMP when released into extracellular space from damaged cells. Extracellular ATP receptors monitor tissue damage and activate a Ca2+ wave in the surrounding healthy cells. How the Ca2+ wave propagates through cells after a wound is unclear. Ca2+ wave activation can occur extracellularly via external receptors or intracellularly through GAP junctions. Three potential mechanisms to propagate the Ca2+ wave are source and sink, amplifying wave, and release and diffusion. Both source and sink and amplifying wave regulate ATP levels using hydrolysis or secretion, respectively, whereas release and diffusion relies on dilution. Here we systematically test these hypotheses using a microfluidics assay to mechanically wound an epithelial monolayer in combination with direct manipulation of ATP hydrolysis and release. We show that a release and diffusion model sufficiently explains Ca2+-wave propagation after an epithelial wound. A release and diffusion model combines the benefits of fast activation at short length scales with a self-limiting response to prevent unnecessary inflammatory responses harmful to the organism.
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Jørgensen, Niklas R., Steven T. Geist, Roberto Civitelli, and Thomas H. Steinberg. "ATP- and Gap Junction–dependent Intercellular Calcium Signaling in Osteoblastic Cells." Journal of Cell Biology 139, no. 2 (October 20, 1997): 497–506. http://dx.doi.org/10.1083/jcb.139.2.497.
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Many cells coordinate their activities by transmitting rises in intracellular calcium from cell to cell. In nonexcitable cells, there are currently two models for intercellular calcium wave propagation, both of which involve release of inositol trisphosphate (IP3)- sensitive intracellular calcium stores. In one model, IP3 traverses gap junctions and initiates the release of intracellular calcium stores in neighboring cells. Alternatively, calcium waves may be mediated not by gap junctional communication, but rather by autocrine activity of secreted ATP on P2 purinergic receptors. We studied mechanically induced calcium waves in two rat osteosarcoma cell lines that differ in the gap junction proteins they express, in their ability to pass microinjected dye from cell to cell, and in their expression of P2Y2 (P2U) purinergic receptors. ROS 17/2.8 cells, which express the gap junction protein connexin43 (Cx43), are well dye coupled, and lack P2U receptors, transmitted slow gap junction-dependent calcium waves that did not require release of intracellular calcium stores. UMR 106-01 cells predominantly express the gap junction protein connexin 45 (Cx45), are poorly dye coupled, and express P2U receptors; they propagated fast calcium waves that required release of intracellular calcium stores and activation of P2U purinergic receptors, but not gap junctional communication. ROS/P2U transfectants and UMR/Cx43 transfectants expressed both types of calcium waves. Gap junction–independent, ATP-dependent intercellular calcium waves were also seen in hamster tracheal epithelia cells. These studies demonstrate that activation of P2U purinergic receptors can propagate intercellular calcium, and describe a novel Cx43-dependent mechanism for calcium wave propagation that does not require release of intracellular calcium stores by IP3. These studies suggest that gap junction communication mediated by either Cx43 or Cx45 does not allow passage of IP3 well enough to elicit release of intracellular calcium stores in neighboring cells.
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Alavi, Sayyed Mohammad Hadi, Ian A. E. Butts, Azadeh Hatef, Maren Mommens, Edward A. Trippel, Matthew K. Litvak, and Igor Babiak. "Sperm morphology, ATP content, and analysis of motility in Atlantic halibut (Hippoglossus hippoglossus)." Canadian Journal of Zoology 89, no. 3 (March 2011): 219–28. http://dx.doi.org/10.1139/z10-113.
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Spermatozoon of Atlantic halibut ( Hippoglossus hippoglossus (L., 1758)) is uniflagellated, lacks an acrosome, and is differentiated into a head, midpiece, and flagellum. There are two to five mitochondria in the midpiece, as well as proximal and distal centrioles. The flagellum consisted of 9 + 2 microtubules surrounded by plasma membrane, which is extended at the proximal part of the flagellum owing to the presence of vacuoles. After sperm activation in seawater, sperm motility and velocity decreased from 98.4% ± 3.4% and 170.3 ± 8.9 µm·s–1 at 15 s after sperm activation to 4.8% ± 4.7% and 9.2 ± 8.9 µm·s–1 at 120 s after sperm activation, respectively. ATP content (nmol·L–1 ATP per 108 spermatozoa) significantly decreased at 60 s after sperm activation (5.9 ± 1.5) compared with at 0 and 30 s after sperm activation (14.9 ± 1.5 and 14.5 ± 1.5, respectively). Beating waves propagated along the full length of the flagellum after sperm activation, whereas waves were restricted to the proximal section during the latter motility period. Wave amplitude significantly decreased at 45 s after sperm activation, but wavelength did not differ. The present study showed associations among sperm morphology, ATP content, flagellar wave parameters, and sperm velocity, which could be used in comparative spermatology.
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Albright, Ronald A., William C. Chang, Donna Robert, Deborah L. Ornstein, Wenxiang Cao, Lynn Liu, Meredith E. Redick, J. Isaac Young, Enrique M. De La Cruz, and Demetrios T. Braddock. "NPP4 is a procoagulant enzyme on the surface of vascular endothelium." Blood 120, no. 22 (November 22, 2012): 4432–40. http://dx.doi.org/10.1182/blood-2012-04-425215.
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Abstract Ap3A is a platelet-dense granule component released into the extracellular space during the second wave of platelet aggregation on activation. Here, we identify an uncharacterized enzyme, nucleotide pyrophosphatase/phosphodiesterase-4 (NPP4), as a potent hydrolase of Ap3A capable of stimulating platelet aggregation and secretion. We demonstrate that NPP4 is present on the surface of vascular endothelium, where it hydrolyzes Ap3A into AMP and ADP, and Ap4A into AMP and ATP. Platelet aggregation assays with citrated platelet-rich plasma reveal that the primary and secondary waves of aggregation and dense granule release are strongly induced by nanomolar NPP4 in a concentration-dependent manner in the presence of Ap3A, while Ap3A alone initiates a primary wave of aggregation followed by rapid disaggregation. NPP2 and an active site NPP4 mutant, neither of which appreciably hydrolyzes Ap3A, have no effect on platelet aggregation and secretion. Finally, by using ADP receptor blockade we confirm that NPP4 mediates platelet aggregation via release of ADP from Ap3A and activation of ADP receptors. Collectively, these studies define the biologic and enzymatic basis for NPP4 and Ap3A activity in platelet aggregation in vitro and suggest that NPP4 promotes hemostasis in vivo by augmenting ADP-mediated platelet aggregation at the site of vascular injury.
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Okamoto, KI, and Y. Nakaoka. "RECONSTITUTION OF METACHRONAL WAVES IN CILIATED CORTICAL SHEETS OF PARAMECIUM - ASYMMETRY OF THE CILIARY MOVEMENTS." Journal of Experimental Biology 192, no. 1 (July 1, 1994): 73–81. http://dx.doi.org/10.1242/jeb.192.1.73.
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In conditions in which ciliated cortical sheets prepared from detergent-extracted Paramecium multimicronucleatum cells adhered to glass coverslips on a microscope stage, perfusion of a reactivation medium containing ATP plus cyclic AMP or cyclic GMP generated metachronal waves. An analysis of the ciliary movements that generate these metachronal waves yielded the following results. During the generation of metachronal waves, there were phase differences in the ciliary orientation of adjacent cilia in the direction of wave propagation. Addition of cyclic AMP or cyclic GMP increased the rotational angular velocities during the effective stroke of ciliary beating, but did not increase the rotational angular velocity of the recovery stroke. When the ATP concentration in the cyclic GMP reactivation medium was increased, the rotational angular velocity during the effective stroke rose steeply and saturated at 0.8 mmol l-1 ATP, whereas that during the recovery stroke rose gradually. Addition of cyclic nucleotides caused a single cilium isolated from neighbouring cilia on the cortical sheet to incline almost parallel to the cortical surface during the recovery stroke. Addition of cyclic GMP increased the amplitude of bending of cilia detached from the cortical sheet. From these results, it was concluded that increases in the asymmetrical movement of individual cilia, caused by the addition of cyclic nucleotides, create the ciliary interaction that generates the metachronal waves.
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Peti-Peterdi, János. "Calcium wave of tubuloglomerular feedback." American Journal of Physiology-Renal Physiology 291, no. 2 (August 2006): F473—F480. http://dx.doi.org/10.1152/ajprenal.00425.2005.
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ATP release from macula densa (MD) cells into the interstitium of the juxtaglomerular (JG) apparatus (JGA) is an integral component of the tubuloglomerular feedback (TGF) mechanism that controls the glomerular filtration rate. Because the cells of the JGA express a number of calcium-coupled purinergic receptors, these studies tested the hypothesis that TGF activation triggers a calcium wave that spreads from the MD toward distant cells of the JGA and glomerulus. Ratiometric calcium imaging of in vitro microperfused isolated JGA-glomerulus complex dissected from rabbits was performed with fluo-4/fura red and confocal fluorescence microscopy. Activation of TGF by increasing tubular flow rate at the MD rapidly produced a significant elevation in intracellular Ca2+ concentration ([Ca2+]i) in extraglomerular mesangial cells (by 187.6 ± 45.1 nM) and JG renin granular cells (by 281.4 ± 66.6 nM). Subsequently, cell-to-cell propagation of the calcium signal at a rate of 12.6 ± 1.1 μm/s was observed upstream toward proximal segments of the afferent arteriole and adjacent glomeruli, as well as toward intraglomerular elements including the most distant podocytes (5.9 ± 0.4 μm/s). The same calcium wave was observed in nonperfusing glomeruli, causing vasoconstriction and contractions of the glomerular tuft. Gap junction uncoupling, an ATP scavenger enzyme cocktail, and pharmacological inhibition of P2 purinergic receptors, but not adenosine A1 receptor blockade, abolished the changes in [Ca2+]i and propagation of the calcium wave. These studies provided evidence that both gap junctional communication and extracellular ATP are integral components of the TGF calcium wave.
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Forcaia, Greta, Beatrice Formicola, Giulia Terribile, Sharon Negri, Dmitry Lim, Gerardo Biella, Francesca Re, Francesco Moccia, and Giulio Sancini. "Multifunctional Liposomes Modulate Purinergic Receptor-Induced Calcium Wave in Cerebral Microvascular Endothelial Cells and Astrocytes: New Insights for Alzheimer’s disease." Molecular Neurobiology 58, no. 6 (January 29, 2021): 2824–35. http://dx.doi.org/10.1007/s12035-021-02299-9.
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AbstractIn light of previous results, we assessed whether liposomes functionalized with ApoE-derived peptide (mApoE) and phosphatidic acid (PA) (mApoE-PA-LIP) impacted on intracellular calcium (Ca2+) dynamics in cultured human cerebral microvascular endothelial cells (hCMEC/D3), as an in vitro human blood-brain barrier (BBB) model, and in cultured astrocytes. mApoE-PA-LIP pre-treatment actively increased both the duration and the area under the curve (A.U.C) of the ATP-evoked Ca2+ waves in cultured hCMEC/D3 cells as well as in cultured astrocytes. mApoE-PA-LIP increased the ATP-evoked intracellular Ca2+ waves even under 0 [Ca2+]e conditions, thus indicating that the increased intracellular Ca2+ response to ATP is mainly due to endogenous Ca2+ release. Indeed, when Sarco-Endoplasmic Reticulum Calcium ATPase (SERCA) activity was blocked by cyclopiazonic acid (CPA), the extracellular application of ATP failed to trigger any intracellular Ca2+ waves, indicating that metabotropic purinergic receptors (P2Y) are mainly involved in the mApoE-PA-LIP-induced increase of the Ca2+ wave triggered by ATP. In conclusion, mApoE-PA-LIP modulate intracellular Ca2+ dynamics evoked by ATP when SERCA is active through inositol-1,4,5-trisphosphate-dependent (InsP3) endoplasmic reticulum Ca2+ release. Considering that P2Y receptors represent important pharmacological targets to treat cognitive dysfunctions, and that P2Y receptors have neuroprotective effects in neuroinflammatory processes, the enhancement of purinergic signaling provided by mApoE-PA-LIP could counteract Aβ-induced vasoconstriction and reduction in cerebral blood flow (CBF). Our obtained results could give an additional support to promote mApoE-PA-LIP as effective therapeutic tool for Alzheimer’s disease (AD).
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Mathiesen, Claus, Alexey Brazhe, Kirsten Thomsen, and Martin Lauritzen. "Spontaneous Calcium Waves in Bergman Glia Increase with Age and Hypoxia and may Reduce Tissue Oxygen." Journal of Cerebral Blood Flow & Metabolism 33, no. 2 (December 5, 2012): 161–69. http://dx.doi.org/10.1038/jcbfm.2012.175.
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Glial calcium (Ca2+) waves constitute a means to spread signals between glial cells and to neighboring neurons and blood vessels. These waves occur spontaneously in Bergmann glia (BG) of the mouse cerebellar cortex in vivo. Here, we tested three hypotheses: (1) aging and reduced blood oxygen saturation alters wave activity; (2) glial Ca2+ waves change cerebral oxygen metabolism; and (3) neuronal and glial wave activity is correlated. We used two-photon microscopy in the cerebellar cortexes of adult (8- to 15-week-old) and aging (48- to 80-week-old) ketamine-anesthetized mice after bolus loading with OGB-1/AM and SR101. We report that the occurrence of spontaneous waves is 20 times more frequent in the cerebellar cortex of aging as compared with adult mice, which correlated with a reduction in resting brain oxygen tension. In adult mice, spontaneous glial wave activity increased on reducing resting brain oxygen tension, and ATP-evoked glial waves reduced the tissue O2 tension. Finally, although spontaneous Purkinje cell (PC) activity was not associated with increased glia wave activity, spontaneous glial waves did affect intracellular Ca2+ activity in PCs. The increased wave activity during aging, as well as low resting brain oxygen tension, suggests a relationship between glial waves, brain energy homeostasis, and pathology.
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Matthus, Elsa, Jian Sun, Limin Wang, Madhura G. Bhat, Amirah B. Mohammad-Sidik, Katie A. Wilkins, Nathalie Leblanc-Fournier, et al. "DORN1/P2K1 and purino-calcium signalling in plants: making waves with extracellular ATP." Annals of Botany 124, no. 7 (November 27, 2019): 1227–42. http://dx.doi.org/10.1093/aob/mcz135.
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Abstract Background and Aims Extracellular ATP governs a range of plant functions, including cell viability, adaptation and cross-kingdom interactions. Key functions of extracellular ATP in leaves and roots may involve an increase in cytosolic free calcium as a second messenger (‘calcium signature’). The main aim here was to determine to what extent leaf and root calcium responses require the DORN1/P2K1 extracellular ATP receptor in Arabidopsis thaliana. The second aim was to test whether extracellular ATP can generate a calcium wave in the root. Methods Leaf and root responses to extracellular ATP were reviewed for their possible links to calcium signalling and DORN1/P2K1. Leaves and roots of wild type and dorn1 plants were tested for cytosolic calcium increase in response to ATP, using aequorin. The spatial abundance of DORN1/P2K1 in the root was estimated using green fluorescent protein. Wild type roots expressing GCaMP3 were used to determine the spatial variation of cytosolic calcium increase in response to extracellular ATP. Key Results Leaf and root ATP-induced calcium signatures differed markedly. The leaf signature was only partially dependent on DORN1/P2K1, while the root signature was fully dependent. The distribution of DORN1/P2K1 in the root supports a key role in the generation of the apical calcium signature. Root apical and sub-apical calcium signatures may operate independently of each other but an apical calcium increase can drive a sub-apical increase, consistent with a calcium wave. Conclusion DORN1 could underpin several calcium-related responses but it may not be the only receptor for extracellular ATP in Arabidopsis. The root has the capacity for a calcium wave, triggered by extracellular ATP at the apex.
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Toma, Ildikó, Eric Bansal, Elliott J. Meer, Jung Julie Kang, Sarah L. Vargas, and János Peti-Peterdi. "Connexin 40 and ATP-dependent intercellular calcium wave in renal glomerular endothelial cells." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 6 (June 2008): R1769—R1776. http://dx.doi.org/10.1152/ajpregu.00489.2007.
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Endothelial intracellular calcium ([Ca2+]i) plays an important role in the function of the juxtaglomerular vasculature. The present studies aimed to identify the existence and molecular elements of an endothelial calcium wave in cultured glomerular endothelial cells (GENC). GENCs on glass coverslips were loaded with Fluo-4/Fura red, and ratiometric [Ca2+]iimaging was performed using fluorescence confocal microscopy. Mechanical stimulation of a single GENC caused a nine-fold increase in [Ca2+]i, which propagated from cell to cell throughout the monolayer (7.9 ± 0.3 μm/s) in a regenerative manner (without decrement of amplitude, kinetics, and speed) over distances >400 μm. Inhibition of voltage-dependent calcium channels with nifedipine had no effect on the above parameters, but the removal of extracellular calcium reduced Δ[Ca2+]iby 50%. Importantly, the gap junction uncoupler α-glycyrrhetinic acid or knockdown of connexin 40 (Cx40) by transfecting GENCs with Cx40 short interfering RNA (siRNA) almost completely eliminated Δ[Ca2+]iand the calcium wave. Breakdown of extracellular ATP using a scavenger cocktail (apyrase and hexokinase) or nonselective inhibition of purinergic P2 receptors with suramin, had similar blocking effects. Scraping cells off along a line eliminated physical contact between cells but did not effect calcium wave propagation. Using an ATP biosensor technique, we detected a significant elevation in extracellular ATP (Δ = 76 ± 2 μM) during calcium wave propagation, which was abolished by Cx40 siRNA treatment (Δ = 6 ± 1 μM). These studies suggest that connexin 40 hemichannels and extracellular ATP are key molecular elements of the glomerular endothelial calcium wave, which may serve important juxtaglomerular functions.
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Ceriani, Federico, Tullio Pozzan, and Fabio Mammano. "Critical role of ATP-induced ATP release for Ca2+ signaling in nonsensory cell networks of the developing cochlea." Proceedings of the National Academy of Sciences 113, no. 46 (November 2, 2016): E7194—E7201. http://dx.doi.org/10.1073/pnas.1616061113.
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Spatially and temporally coordinated variations of the cytosolic free calcium concentration ([Ca2+]c) play a crucial role in a variety of tissues. In the developing sensory epithelium of the mammalian cochlea, elevation of extracellular adenosine trisphosphate concentration ([ATP]e) triggers [Ca2+]c oscillations and propagation of intercellular inositol 1,4,5-trisphosphate (IP3)-dependent Ca2+ waves. What remains uncertain is the relative contribution of gap junction channels and connexin hemichannels to these fundamental mechanisms, defects in which impair hearing acquisition. Another related open question is whether [Ca2+]c oscillations require oscillations of the cytosolic IP3 concentration ([IP3]c) in this system. To address these issues, we performed Ca2+ imaging experiments in the lesser epithelial ridge of the mouse cochlea around postnatal day 5 and constructed a computational model in quantitative adherence to experimental data. Our results indicate that [Ca2+]c oscillations are governed by Hopf-type bifurcations within the experimental range of [ATP]e and do not require [IP3]c oscillations. The model replicates accurately the spatial extent and propagation speed of intercellular Ca2+ waves and predicts that ATP-induced ATP release is the primary mechanism underlying intercellular propagation of Ca2+ signals. The model also uncovers a discontinuous transition from propagating regimes (intercellular Ca2+ wave speed > 11 μm⋅s−1) to propagation failure (speed = 0), which occurs upon lowering the maximal ATP release rate below a minimal threshold value. The approach presented here overcomes major limitations due to lack of specific connexin channel inhibitors and can be extended to other coupled cellular systems.
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Boitano, Scott, and W. Howard Evans. "Connexin mimetic peptides reversibly inhibit Ca2+signaling through gap junctions in airway cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 4 (October 1, 2000): L623—L630. http://dx.doi.org/10.1152/ajplung.2000.279.4.l623.
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The effect of peptides with sequences derived from connexins, the constituent proteins of gap junctions, on mechanically stimulated intercellular Ca2+signaling in tracheal airway epithelial cells was studied. Three peptides with sequences corresponding to connexin extracellular loop regions reversibly restricted propagation of Ca2+ waves to neighboring cells. Recovery of communication began within 10 min of removal of the peptides, with inhibition totally reversed by 20–40 min. The peptides were shown to be more effective in inhibiting Ca2+ waves than glycyrrhetinic acid or oleamide. Inhibition of intercellular Ca2+ waves by connexin mimetic peptides did not affect the Ca2+ response to extracellular ATP. Although the intracellular Ca2+ response of tracheal epithelial cells to ATP was greatly reduced by either pretreatment with high doses of ATP or application of apyrase, mechanically stimulated intercellular Ca2+ signaling was not affected by these agents. We conclude that connexin mimetic peptides are effective and reversible inhibitors of gap junctional communication of physiologically significant molecules that underlie Ca2+wave propagation in tracheal epithelial cells and propose a potential mechanism for the mode of action of mimetic peptides.
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Baranov, M. I. "Calculation of Basic Average Drift Characteristics of Free Electrons in a Metallic Conductor with Electric Current." Elektronnaya Obrabotka Materialov 58, no. 1 (February 2022): 79–84. http://dx.doi.org/10.52577/eom.2022.58.1.79.
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The results of an approximate calculation of theaveraged values of speeds of vmz of a longi-tudinal drift of lone electrons, and of circular frequencies of ωmz change of longitudinal elec-tronic waves de Broglie and of lengths of λmz of longitudinal electronic waves de Broglie in the metal of round cylindrical conductor with an electric axial-flow current of conductivity of i0(t) of different kinds (permanent, variable, and impulsive) and amplitude-time parameters (ATP). The results of verification of the obtained calculation correlations for speeds of vmz drift of lone electrons and lengths of λmz of electronic de Broglie waves in the examined con-ductor demonstrate their validity and working capacity. The obtained data confirm the quan-tum-wave nature of the electric current of conductivity of the indicated kinds of i0(t) and of ATP in a metallic conductor.
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Zima, Aleksey V., Malikarjuna R. Pabbidi, Stephen L. Lipsius, and Lothar A. Blatter. "Effects of mitochondrial uncoupling on Ca2+ signaling during excitation-contraction coupling in atrial myocytes." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 7 (April 1, 2013): H983—H993. http://dx.doi.org/10.1152/ajpheart.00932.2012.
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Mitochondria play an important role in intracellular Ca2+ concentration ([Ca2+]i) regulation in the heart. We studied sarcoplasmic reticulum (SR) Ca2+ release in cat atrial myocytes during depolarization of mitochondrial membrane potential (ΔΨm) induced by the protonophore FCCP. FCCP caused an initial decrease of action potential-induced Ca2+ transient amplitude and frequency of spontaneous Ca2+ waves followed by partial recovery despite partially depleted SR Ca2+ stores. In the presence of oligomycin, FCCP only exerted a stimulatory effect on Ca2+ transients and Ca2+ wave frequency, suggesting that the inhibitory effect of FCCP was mediated by ATP consumption through reverse-mode operation of mitochondrial F1F0-ATPase. ΔΨm depolarization was accompanied by cytosolic acidification, increases of diastolic [Ca2+]i, intracellular Na+ concentration ([Na+]i), and intracellular Mg2+ concentration ([Mg2+]i), and a decrease of intracellular ATP concentration ([ATP]i); however, glycolytic ATP production partially compensated for the exhaustion of mitochondrial ATP supplies. In conclusion, the initial inhibition of Ca2+ transients and waves resulted from suppression of ryanodine receptor SR Ca2+ release channel activity by a decrease in [ATP], an increase of [Mg2+]i, and cytoplasmic acidification. The later stimulation resulted from reduced mitochondrial Ca2+ buffering and cytosolic Na+ and Ca2+ accumulation, leading to enhanced Ca2+-induced Ca2+ release and spontaneous Ca2+ release in the form of Ca2+ waves. ΔΨm depolarization and the ensuing consequences of mitochondrial uncoupling observed here (intracellular acidification, decrease of [ATP]i, increase of [Na+]i and [Mg2+]i, and Ca2+ overload) are hallmarks of ischemia. These findings may therefore provide insight into the consequences of mitochondrial uncoupling for ion homeostasis, SR Ca2+ release, and excitation-contraction coupling in ischemia at the cellular and subcellular level.
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Mazzarda, Flavia, Annunziata D'Elia, Roberto Massari, Adele De Ninno, Francesca Romana Bertani, Luca Businaro, Gaia Ziraldo, et al. "Organ-on-chip model shows that ATP release through connexin hemichannels drives spontaneous Ca2+ signaling in non-sensory cells of the greater epithelial ridge in the developing cochlea." Lab on a Chip 20, no. 16 (2020): 3011–23. http://dx.doi.org/10.1039/d0lc00427h.
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Using microfluidics, ATP biosensors, multiphoton microscopy and genetically targeted mice, we show that ATP release through connexin hemichannels, and not pannexin 1 channels, underlies spontaneous Ca2+ wave propagation in the greater epithelial ridge of the developing cochlea.
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Du, Ling, Tao Shen, Bing Liu, Yunhe Zhang, Cong Zhao, Na Jia, Que Wang, and Qing He. "Shock Wave Therapy Promotes Cardiomyocyte Autophagy and Survival during Hypoxia." Cellular Physiology and Biochemistry 42, no. 2 (2017): 673–84. http://dx.doi.org/10.1159/000477885.
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Background: Autophagy plays an important role in cardiovascular disease. Controversy still exists regarding the effect of autophagy on ischemic/hypoxic myocardium. Cardiac shock wave therapy (CSWT) is an effective alternative treatment for refractory ischemic heart disease. Whether CSWT can regulate cardiomyocyte autophagy under hypoxic conditions is not clear. We established a myocardial hypoxia model using the H9c2 cell line and performed shock waves (SWs) treatment to evaluate the effect of SW on autophagy. Methods: The H9c2 cells were incubated under hypoxic conditions, and SW treatment was then performed at energies of 0.02, 0.05, or 0.10 mJ/mm2. The cell viability and intracellular ATP level were examined. Western blot analysis was used to assess the expression of LC3B, AMPK, mTOR, Beclin-1, Sirt1, and HIF-1α. Autophagic vacuoles were visualized by monodansylcadaverine staining. Results: After the 24-hour hypoxic period, cardiomyocyte viability and ATP levels were decreased and autophagy was significantly increased in H9c2 cells. SW treatment with an energy of 0.05 mJ/mm2 significantly increased the cellular viability, ATP level, LC3B-II/I, and number of autophagic vacuoles. In addition, phosphorylated AMPK and Sirt1 were increased and phosphorylated mTOR and HIF-1α were decreased after SW treatment. Conclusion: SW treatment can potentially promote cardiomyocyte autophagy during hypoxia and protect cardiomyocyte function by regulating the AMPK/mTOR pathway.
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Darby, Mark, J. Brent Kuzmiski, William Panenka, Denise Feighan, and Brian A. MacVicar. "ATP Released From Astrocytes During Swelling Activates Chloride Channels." Journal of Neurophysiology 89, no. 4 (April 1, 2003): 1870–77. http://dx.doi.org/10.1152/jn.00510.2002.
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ATP release from astrocytes contributes to calcium ([Ca2+]) wave propagation and may modulate neuronal excitability. In epithelial cells and hepatocytes, cell swelling causes ATP release, which leads to the activation of a volume-sensitive Cl− current ( I Cl,swell) through an autocrine pathway involving purinergic receptors. Astrocyte swelling is counterbalanced by a regulatory volume decrease, involving efflux of metabolites and activation of I Cl,swell and K+currents. We used whole cell patch-clamp recordings in cultured astrocytes to investigate the autocrine role of ATP in the activation of I Cl,swell by hypo-osmotic solution (HOS). Apyrase, an ATP/ADP nucleotidase, inhibited HOS-activated I Cl,swell, whereas ATP and the P2Y agonists, ADPβS and ADP, induced Cl− currents similar to I Cl,swell. Neither the P2U agonist, UTP nor the P2X agonist, α,β-methylene ATP, were effective. BzATP was less effective than ATP, suggesting that P2X7 receptors were not involved. P2 purinergic antagonists, suramin, RB2, and pyridoxalphosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS) reversibly inhibited activation of I Cl,swell, suggesting that ATP-activated P2Y1 receptors. Thus ATP release mediates I Cl,swell in astrocytes through the activation of P2Y1-like receptors. The multidrug resistance protein (MRP) transport inhibitors probenicid, indomethacin, and MK-571 all potently inhibited I Cl.swell. ATP release from astrocytes in HOS was observed directly using luciferin-luciferase and MK-571 reversibly depressed this HOS-induced ATP efflux. We conclude that ATP release via MRP and subsequent autocrine activation of purinergic receptors contributes to the activation of I Cl,swell in astrocytes by HOS-induced swelling.
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Jia, Huibin. "An Improved Traveling-Wave-Based Fault Location Method with Compensating the Dispersion Effect of Traveling Wave in Wavelet Domain." Mathematical Problems in Engineering 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/1019591.
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The fault generated transient traveling waves are wide band signals which cover the whole frequency range. When the frequency characteristic of line parameters is considered, different frequency components of traveling wave will have different attenuation values and wave velocities, which is defined as the dispersion effect of traveling wave. Because of the dispersion effect, the rise or fall time of the wavefront becomes longer, which decreases the singularity of traveling wave and makes it difficult to determine the arrival time and velocity of traveling wave. Furthermore, the dispersion effect seriously affects the accuracy and reliability of fault location. In this paper, a novel double-ended fault location method has been proposed with compensating the dispersion effect of traveling wave in wavelet domain. From the propagation theory of traveling wave, a correction function is established within a certain limit band to compensate the dispersion effect of traveling wave. Based on the determined arrival time and velocity of traveling wave, the fault distance can be calculated precisely by utilizing the proposed method. The simulation experiments have been carried out in ATP/EMTP software, and simulation results demonstrate that, compared with the traditional traveling-wave fault location methods, the proposed method can significantly improve the accuracy of fault location. Moreover, the proposed method is insensitive to different fault conditions, and it is adaptive to both transposed and untransposed transmission lines well.
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CAPOZZI, Ilaria, Rossana TONON, and Paola d'ANDREA. "Ca2+-sensitive phosphoinositide hydrolysis is activated in synovial cells but not in articular chondrocytes." Biochemical Journal 344, no. 2 (November 24, 1999): 545–53. http://dx.doi.org/10.1042/bj3440545.
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Cell-to-cell diffusion of second messengers across intercellular channels allows tissues to co-ordinate responses to extracellular stimuli. Intercellular diffusion of inositol 1,4,5-trisphosphate, locally produced by focal stimulations, sustains the propagation of intercellular Ca2+ waves, by stimulating the release of intracellular Ca2+ in neighbouring cells. We previously demonstrated that in cultured articular chondrocytes and HIG-82 synovial cells, studied with digitial fluorescence video imaging, mechanical stimulation of a single cell induced intercellular Ca2+ waves dependent on the presence of gap junctions. In the absence of extracellular Ca2+ the propagating distance of the wave decreased significantly in HIG-82 cells, but appeared unaffected in chondrocytes. We now show that both cells types express connexin 43 and a similar functional coupling, thus suggesting that the different Ca2+ sensitivity of intercellular waves is not due to major differences in gap junction constituent proteins. In HIG-82 synoviocytes, but not in chondrocytes, the Ca2+ ionophore ionomycin stimulated phosphoinositide hydrolysis in a concentration-dependent manner, an effect strictly dependent on the presence of extracellular Ca2+, suggesting the expression, in these cells, of a Ca2+-sensitive phospholipase C activity. Such an activity could be stimulated also by Ca2+ influx induced by P2Y receptor activation and considerably amplifies ATP-induced inositol phosphate (InsP) production. In contrast, Ca2+ influx did not affect considerably the response of chondrocytes to ATP stimulation. In HIG-82 cells, the combined application of ionomycin and ATP maximally stimulated InsP synthesis, suggesting the involvement of two independent mechanisms in inositol phosphate generation. These results suggest that in HIG-82 synovial cells the recruitment of a Ca2+-sensitive phospholipase C activity could amplify the cell response to a focally applied extracellular stimulus, thus providing a positive feedback mechanism for intercellular wave propagation.
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Balemba, Onesmo B., Aaron C. Bartoo, Mark T. Nelson, and Gary M. Mawe. "Role of mitochondria in spontaneous rhythmic activity and intracellular calcium waves in the guinea pig gallbladder smooth muscle." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 2 (February 2008): G467—G476. http://dx.doi.org/10.1152/ajpgi.00415.2007.
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Mitochondrial Ca2+ handling has been implicated in spontaneous rhythmic activity in smooth muscle and interstitial cells of Cajal. In this investigation we evaluated the effect of mitochondrial inhibitors on spontaneous action potentials (APs), Ca2+ flashes, and Ca2+ waves in gallbladder smooth muscle (GBSM). Disruption of the mitochondrial membrane potential with carbonyl cyanide 3-chlorophenylhydrazone, carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone, rotenone, and antimycin A significantly reduced or eliminated APs, Ca2+ flashes, and Ca2+ waves in GBSM. Blockade of ATP production with oligomycin did not alter APs or Ca2+ flashes but significantly reduced Ca2+ wave frequency. Inhibition of mitochondrial Ca2+ uptake and Ca2+ release with Ru360 and CGP-37157, respectively, reduced the frequency of Ca2+ flashes and Ca2+ waves in GBSM. Similar to oligomycin, cyclosporin A did not alter AP and Ca2+ flash frequency but significantly reduced Ca2+ wave activity. These data suggest that mitochondrial Ca2+ handling is necessary for the generation of spontaneous electrical activity and may therefore play an important role in gallbladder tone and motility.
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Emonnot, Léa, Charles Bakhos, Bruno Chapuis, Valérie Oréa, Christian Barrès, and Claude Julien. "Role of purinergic cotransmission in the sympathetic control of arterial pressure variability in conscious rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 3 (September 2006): R736—R741. http://dx.doi.org/10.1152/ajpregu.00088.2006.
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Previous studies have shown that the sympathetically mediated oscillations of arterial pressure (AP), the so-called Mayer waves, are shifted from 0.4 to 0.6 Hz after acute α-adrenoceptor blockade in conscious rats. This raises the possibility that, under physiological conditions, Mayer waves are mediated by the conjoint action of norepinephrine and other sympathetic cotransmitters. To evaluate the possible role of the cotransmitter ATP in determining the frequency of Mayer waves, AP and renal sympathetic nerve activity (RSNA) were simultaneously recorded in 10 conscious rats with cardiac autonomic blockade before and after acute blockade of P2 receptors with pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid. P2 receptor blockade did not alter the mean level and overall variability of AP and RSNA but shifted peak coherence between AP and RSNA from 0.43 ± 0.02 to 0.22 ± 0.01 Hz. A model of the sympathetic limb of the arterial baroreceptor reflex was designed to simulate Mayer waves at 0.2 and 0.6 Hz, with norepinephrine and ATP, respectively, acting as the sole sympathetic cotransmitter. When both cotransmitters acted in concert, a single oscillation was observed at 0.4 Hz when the gain ratio of the adrenergic to the purinergic components was set at 15. The model thus accounted for an important role for ATP in determining Mayer wave frequency, but not in sustaining the mean level of AP or controlling its overall variability.
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Isakson, Brant E., W. Howard Evans, and Scott Boitano. "Intercellular Ca2+ signaling in alveolar epithelial cells through gap junctions and by extracellular ATP." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 2 (February 1, 2001): L221—L228. http://dx.doi.org/10.1152/ajplung.2001.280.2.l221.
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Inter- and extracellular-mediated changes in intracellular Ca2+concentration ([Ca2+]i) can ensure coordinated tissue function in the lung. Cultured rat alveolar epithelial cells (AECs) have been shown to respond to secretagogues with increases in [Ca2+]i and have been shown to be gap junctionally coupled. However, communication of [Ca2+]i changes in AECs is not well defined. Monolayers of AECs were mechanically perturbed and monitored for [Ca2+]i changes. Perturbation of AECs was administered by a glass probe to either mechanically stimulate or mechanically wound individual cells. Both approaches induced a change in [Ca2+]i in the stimulated cell that was propagated to neighboring cells (Ca2+ waves). A connexin mimetic peptide shown to uncouple gap junctions eliminated Ca2+ waves in mechanically stimulated cells but had no effect on mechanically wounded cells. In contrast, apyrase, an enzyme that effectively removes ATP from the extracellular milieu, had no effect on mechanically stimulated cells but severely restricted mechanically wounded Ca2+ wave propagation. We conclude that AECs have the ability to communicate coordinated Ca2+ changes using both gap junctions and extracellular ATP.
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Wang, Jing, Xiao Liu, and Zhi Yuan Pan. "A New Fault Location Method for Distribution Network Based on Traveling Wave Theory." Advanced Materials Research 1070-1072 (December 2014): 718–25. http://dx.doi.org/10.4028/www.scientific.net/amr.1070-1072.718.
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The conventional approaches to distribution network fault location has certain drawbacks in terms of complexity, especially the fault occurred in the branch lines. In this paper, a novel fault location method based on D-type traveling wave was proposed. This method choose the measurement point which the initial traveling waves first reached as the reference measurement point, and the distance between multiple failure points received a fault traveling wave signal to the reference measurement point was calculated. Then, the maximum distance between multiple failure points to the reference measurement point was selected as location of the final failure point. The simulation result with ATP simulation software and MATLAB software show that the proposed method can achieve fault location fast and accurately within a very short period. Compared with the existing algorithms, this method was consistent whether the fault occurred in the main line or branch lines, which improved the accuracy and reliability of the traveling wave fault location in distribution network.
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Hansen, M., S. Boitano, E. R. Dirksen, and M. J. Sanderson. "A role for phospholipase C activity but not ryanodine receptors in the initiation and propagation of intercellular calcium waves." Journal of Cell Science 108, no. 7 (July 1, 1995): 2583–90. http://dx.doi.org/10.1242/jcs.108.7.2583.
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Mechanical stimulation of a single cell in an airway epithelial culture initiates an increase in intracellular Ca2+ concentration ([Ca2+]i) that propagates from cell to cell as an intercellular Ca2+ wave. These Ca2+ waves appear to require an increase in intracellular inositol 1,4,5-trisphosphate (IP3) concentration ([IP3]i) in the stimulated cell and are propagated between cells by the diffusion of IP3 through gap junctions. To test the hypothesis that the activation of phospholipase C (PLC) contributes to the elevation of [IP3]i and initiation of an intercellular Ca2+ wave, changes in [Ca2+]i induced by mechanical stimulation were measured by digital fluorescence microscopy in the presence of the PLC inhibitor, aminosteroid U73122. Following exposure to U73122 mechanical stimulation elevated [Ca2+]i of the stimulated cell, but did not initiate the propagation of an intercellular Ca2+ wave. By contrast, in the presence of U73343, a similar aminosteroid that does not inactivate PLC, mechanical stimulation increased the [Ca2+]i of the stimulated cell and initiated an intercellular Ca2+ wave. U73122 also blocked the elevation of [Ca2+]i of airway epithelial cells in response to ATP, a P2-receptor agonist that activates PLC to elevate [IP3]i and [Ca2+]i. In addition, the propagation of intercellular Ca2+ waves was not affected by the ryanodine-receptor agonists, caffeine or ryanodine. The hypotheses that: (1) an elevation of [IP3]i is required to initiate intercellular Ca2+ waves; (2) mechanical stimulation activates PLC; and (3) Ca2+ wave propagation in airway epithelial cells involves Ca2+ release from intracellular stores primarily via IP3 receptors are supported by these results.
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Terasaki, M., and C. Sardet. "Demonstration of calcium uptake and release by sea urchin egg cortical endoplasmic reticulum." Journal of Cell Biology 115, no. 4 (November 15, 1991): 1031–37. http://dx.doi.org/10.1083/jcb.115.4.1031.
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The calcium indicator dye fluo-3/AM was loaded into the ER of isolated cortices of unfertilized eggs of the sea urchin Arbacia punctulata. Development of the fluorescent signal took from 8 to 40 min and usually required 1 mM ATP. The signal decreased to a minimum level within 30 s after perfusion with 1 microM InsP3 and increased within 5 min when InsP3 was replaced with 1 mM ATP. Also, the fluorescence signal was lowered rapidly by perfusion with 10 microM A23187 or 10 microM ionomycin. These findings demonstrate that the cortical ER is a site of ATP-dependent calcium sequestration and InsP3-induced calcium release. A light-induced wave of calcium release, traveling between 0.7 and 2.8 microns/s (average speed 1.4 microns/s, N = 8), was sometimes observed during time lapse recordings; it may therefore be possible to use the isolated cortex preparation to investigate the postfertilization calcium wave.
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Evans, John H., and Michael J. Sanderson. "Intracellular calcium oscillations induced by ATP in airway epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 277, no. 1 (July 1, 1999): L30—L41. http://dx.doi.org/10.1152/ajplung.1999.277.1.l30.
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In airway epithelial cells, extracellular ATP (ATPo) stimulates an initial transient increase in intracellular Ca2+ concentration that is followed by periodic increases in intracellular Ca2+ concentration (Ca2+ oscillations). The characteristics and mechanism of these ATP-induced Ca2+ responses were studied in primary cultures of rabbit tracheal cells with digital video fluorescence microscopy and the Ca2+-indicator dye fura 2. The continual presence of ATPo at concentrations of 0.1–100 μM stimulated Ca2+ oscillations that persisted for 20 min. The frequency of the Ca2+ oscillations was found to be dependent on both ATPoconcentration and intrinsic sensitivity of each cell to ATPo. Cells exhibited similar Ca2+ oscillations to extracellular UTP (UTPo), but the oscillations typically occurred at lower UTPoconcentrations. The ATP-induced Ca2+ oscillations were abolished by the phospholipase C inhibitor U-73122 and by the endoplasmic reticulum Ca2+-pump inhibitor thapsigargin but were maintained in Ca2+-free medium. These results are consistent with the hypothesis that in airway epithelial cells ATPo and UTPo act via P2U purinoceptors to stimulate Ca2+ oscillations by the continuous production of inositol 1,4,5-trisphosphate and the oscillatory release of Ca2+ from internal stores. ATP-induced Ca2+oscillations of adjacent individual cells occurred independently of each other. By contrast, a mechanically induced intercellular Ca2+ wave propagated through a field of Ca2+-oscillating cells. Thus Ca2+ oscillations and propagating Ca2+ waves are two fundamental modes of Ca2+signaling that exist and operate simultaneously in airway epithelial cells.
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Woodruff, Michael L., Victor V. Chaban, Christopher M. Worley, and Ellen R. Dirksen. "PKC role in mechanically induced Ca2+ waves and ATP-induced Ca2+ oscillations in airway epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 4 (April 1, 1999): L669—L678. http://dx.doi.org/10.1152/ajplung.1999.276.4.l669.
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Mechanical stimulation of airway epithelial cells generates the Ca2+ mobilization messenger inositol 1,4,5-trisphosphate and the protein kinase (PK) C activator diacylglycerol. Inositol 1,4,5-trisphosphate diffuses through gap junctions to mediate intercellular communication of the mechanical stimulus (a “Ca2+ wave”); the role that diacylglycerol-activated PKC might play in the response is unknown. Using primary cultures of rabbit tracheal cells, we show that 12- O-tetradecanoylphorbol 13-acetate- or 1,2-dioctanyl- sn-glycerol-induced activation of PKC slows the Ca2+wave, decreases the amplitude of induced intracellular free Ca2+ concentration ([Ca2+]i) increases, and decreases the number of affected cells. The PKC inhibitors bisindolylmaleimide and Gö 6976 slowed the spread of the wave but did not change the number of affected cells. We show that ATP-induced [Ca2+]iincreases and oscillations, responses independent of intercellular communication, were inhibited by PKC activators. Bisindolylmaleimide decreased the amplitude of ATP-induced [Ca2+]iincreases and blocked oscillations, suggesting that PKC has an initial positive effect on Ca2+mobilization and then mediates feedback inhibition. PKC activators also reduced the [Ca2+]iincrease that followed thapsigargin treatment, indicating a PKC effect associated with the Ca2+ release mechanism.
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Qin, Jian, Yanjun Peng, Lu Wang, Jianxi Wang, Ningbo Pan, Yongqiang Huang, and Xiaohui Zhang. "Research on inter-turn short circuit fault location of SF6 circuit breaker energy storage motor coil based on traveling wave reflection method." Journal of Physics: Conference Series 2246, no. 1 (April 1, 2022): 012062. http://dx.doi.org/10.1088/1742-6596/2246/1/012062.
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Abstract —The traveling wave reflection method is proposed to locate the inter-turn short circuit fault of the circuit breaker energy storage motor coil. The capacitance and inductance matrices of the energy storage motor coil are calculated by finite element simulation, and the wave impedance model of the coil is established based on ATP-EMTP. The low-voltage square wave pulse signal is injected at the winding head to detect the characteristic curve of reflected wave when inter-turn short circuit fault occurs. The variation law of generalized fractal dimension of reflection wave characteristic curve with short circuit position is analyzed. The short-circuit position is evaluated based on BP neural network, and the evaluation accuracy is 100 %, indicating that this method is feasible.
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Stamatakis, Michail, and Nikos V. Mantzaris. "Modeling of ATP-mediated signal transduction and wave propagation in astrocytic cellular networks." Journal of Theoretical Biology 241, no. 3 (August 2006): 649–68. http://dx.doi.org/10.1016/j.jtbi.2006.01.002.
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Wilde, Arthur A. M. "“J-wave syndromes” bring the ATP-sensitive potassium channel back in the spotlight." Heart Rhythm 9, no. 4 (April 2012): 556–57. http://dx.doi.org/10.1016/j.hrthm.2012.01.002.
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Xu, Yan, Shi Qiu, Di Feng Shi, and Guo Lin Huang. "Travelling Wave Fault Location for Distribute Cable Network Based on Distributed Measurement." Applied Mechanics and Materials 373-375 (August 2013): 976–80. http://dx.doi.org/10.4028/www.scientific.net/amm.373-375.976.
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This template carries out a three-terminal accurate fault location method for distribute cable network. It is improved from type D principle fault location method. Radial distribution network is decomposed into T-type networks. A set of formulas based on three-terminal data can calculate fault distance and find fault branch. Only first transient wave heads is needed. Shorter transmission distance makes it more accurate to extract first wave heads with wavelet. The distributed measurement offers redundant transient voltage data. These data is fully used to improve location success rate and accuracy. The simulation result in ATP-EMTP shows that the location accuracy isnt influenced by wave speed, catadioptric wave, grounding resistance and initial fault phase angle.
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He, Ren Wang, and Yi Bo Yang. "A Novel Transient Directional Unit Based on Adaptive Median Filtering." Advanced Materials Research 433-440 (January 2012): 4500–4505. http://dx.doi.org/10.4028/www.scientific.net/amr.433-440.4500.
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A new transient directional unit for extra high voltage(EHV) power transmission lines is proposed, which identifies fault direction by means of comparing the time-domain transient energy of the forward traveling-wave with that of the backward one in the very short period of time after fault occurs. The unit algorithm is designed with the technology of adaptive median filtering, which is first employed to process the forward and backward traveling-waves, and then calculates the time-domain transient energy ratio of the forward traveling-wave to the back one, by which the fault direction is discriminated. Numerous ATP-EMTP simulation tests show that this proposed directional unit not only operates reliably, sensitively and ultra-high-speed, but also endure the influences of various factors, including different fault types, fault locations, transition resistances or fault inception angles. It will be worthy of application greatly.
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Jiang, Pengchong, Fulin Xing, Bu Guo, Jianyu Yang, Zheming Li, Wei Wei, Fen Hu, et al. "Nucleotide transmitters ATP and ADP mediate intercellular calcium wave communication via P2Y12/13 receptors among BV-2 microglia." PLOS ONE 12, no. 8 (August 11, 2017): e0183114. http://dx.doi.org/10.1371/journal.pone.0183114.
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Klepeis, Veronica E., Ann Cornell-Bell, and Vickery Trinkaus-Randall. "Growth factors but not gap junctions play a role in injury-induced Ca2+ waves in epithelial cells." Journal of Cell Science 114, no. 23 (December 1, 2001): 4185–95. http://dx.doi.org/10.1242/jcs.114.23.4185.
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This paper characterizes the early responses of epithelial cells to injury. Ca2+ is an important early messenger that transiently increases in the cytoplasm of cells in response to external stimuli. Its elevation leads to the regulation of signaling pathways responsible for the downstream events important for wound repair, such as cell migration and proliferation. Live cell imaging in combination with confocal laser scanning microscopy of fluo-3 AM loaded cells was performed. We found that mechanical injury in a confluent region of cells creates an elevation in Ca2+ that is immediately initiated at the wound edge and travels as a wave to neighboring cells, with [Ca2+]i returning to background levels within two minutes. Addition of epidermal growth factor (EGF), but not platelet-derived growth factor-BB, resulted in increased [Ca2+]i, and EGF specifically enhanced the amplitude and duration of the injury-induced Ca2+ wave. Propagation of the Ca2+ wave was dependent on intracellular Ca2+ stores, as was demonstrated using both thapsigargin and Ca2+ chelators (EGTA and BAPTA/AM). Injury-induced Ca2+ waves were not mediated via gap junctions, as the gap-junction inhibitors 1-heptanol and 18α-glycyrrhetinic acid did not alter wave propagation, nor did the cells recover in photobleaching experiments. Additional studies also demonstrated that the wave could propagate across an acellular region. The propagation of the injury-induced Ca2+ wave occurs via diffusion of an extracellular mediator, most probably via a nucleotide such as ATP or UTP, that is released upon cell damage. Movies available on-line
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Motoyama, Kentaro, Irene E. Karl, M. Wayne Flye, Dale F. Osborne, and Richard S. Hotchkiss. "Effect of Ca2+ agonists in the perfused liver: determination via laser scanning confocal microscopy." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 2 (February 1, 1999): R575—R585. http://dx.doi.org/10.1152/ajpregu.1999.276.2.r575.
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Ca2+is a critical intracellular second messenger, but few studies have examined Ca2+ signaling in whole organs. The amplitude and frequency of Ca2+ oscillations encode important cellular information. Using laser scanning confocal microscopy in the indo 1 acetoxymethyl ester dye-loaded rat liver, we investigated the effect of various Ca2+ agonists that act at distinct mechanistic sites on Ca2+ signaling. Perfusion with suprathreshold doses of arginine vasopressin (AVP) (2–20 nM) caused a single Ca2+ wave that originated in the pericentral vein region and spread centrifugally to the periportal area. Lower doses of AVP (0.2–2 nM) caused multiple Ca2+ waves and Ca2+ oscillations. Perfusion with ATP (1.4–17.5 μM) caused rapid transient elevations in intracellular free Ca2+concentration ([Ca2+]i) occurring in isolated hepatocytes or groups of hepatocytes throughout the lobule and were of shorter duration than those due to AVP. Also in contrast to AVP, there was no specific anatomic location within the hepatic lobule that was more susceptible to ATP. Thapsigargin and cyclopiazonic acid did not cause a Ca2+ wave but rather produced a uniform and fairly simultaneous increase in [Ca2+]iin all hepatocytes in the lobule. Perfusion with 14 μM ryanodine produced a single transient spike in [Ca2+]iin a small number (<2%) of hepatocytes. Dantrolene, an inhibitor of Ca2+ release, reduced the increased [Ca2+]ioccurring after AVP. Insight into the mechanism of action of these Ca2+-active compounds on Ca2+ signaling in the intact liver is provided.
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Haughey, Norman J., and Mark P. Mattson. "Alzheimer's Amyloid β-Peptide Enhances ATP/Gap Junction-Mediated Calcium-Wave Propagation in Astrocytes." NeuroMolecular Medicine 3, no. 3 (2003): 173–80. http://dx.doi.org/10.1385/nmm:3:3:173.
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Hamaoka, T., H. Iwane, T. Shimomitsu, T. Katsumura, N. Murase, S. Nishio, T. Osada, Y. Kurosawa, and B. Chance. "Noninvasive measures of oxidative metabolism on working human muscles by near-infrared spectroscopy." Journal of Applied Physiology 81, no. 3 (September 1, 1996): 1410–17. http://dx.doi.org/10.1152/jappl.1996.81.3.1410.
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The purpose of this study was to determine whether the initial rate of hemoglobin and myoglobin deoxygenation during immediate postexercise ischemia, a reflection of muscle O2 consumption (VO2mus), can be a quantitative measure of muscle oxidative metabolism. The finger flexor muscles of five healthy men (aged 25-31 yr) were monitored by 31P-magnetic resonance spectroscopy for changes in phosphocreatine (PCr), Pi, and pH. Tests were conducted during 15 min of cuff ischemia and during 5 min of submaximal isotonic grip exercise at 10, 20, 30, and 40% of maximal voluntary contraction, one contraction every 4 s. The VO2mus changes were also monitored by near-infrared spectroscopy with continuous wave. The VO2mus during exercise was expressed relative to the resting value. The resting metabolic rate, calculated from the PCr breakdown rate after complete O2 depletion, was 0.0010 (SD) mM ATP/s. During submaximal exercise (pH > 6.9), the VO2mus increased with a rise in intensity (0.036 +/- 0.011, 0.054 +/- 0.016, 0.062 +/- 0.012, and 0.067 +/- 0.020 mM ATP/s during 10, 20, 30, and 40% maximal voluntary contraction, respectively) and showed significant correlation with changes in both calculated ADP and PCr values (r2 = 0.98 and r2 = 0.99, respectively). In conclusion, because of the significant correlation with regulatory metabolites (ADP and PCr) of oxidative phosphorylation, O2 decline rate in immediate postexercise ischemia determined by near-infrared spectroscopy with continuous wave can be utilized for the quantitative evaluation of localized muscle oxidative metabolism.
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Qian, Shuaiwei, Lu Wang, Jianxi Chen, Yanjun Peng, Ningbo Pan, Yongqiang Huang, and Xiong Zhou. "Research on Fault Location of SF6 Circuit Breaker Relay Coil Based on Traveling-Wave Reflection Method." Journal of Physics: Conference Series 2246, no. 1 (April 1, 2022): 012059. http://dx.doi.org/10.1088/1742-6596/2246/1/012059.
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Abstract —The traveling wave-reflection method is proposed to locate the short circuit fault of the opening/closing coil of the circuit breaker, the capacitance and inductance matrix of the opening/closing coil are calculated by finite element simulation, and the wave impedance model of the coil is established based on ATP-EMTP. A low-voltage square wave pulse signal is injected into the head end of the winding to detect the characteristic curve of the reflected wave when an inter-turn short-circuit fault occurs. The generalized fractal dimension of reflection wave characteristic curve was calculated and its variation as the position of short circuit change was analysed. Compared with box dimension, the variation of information dimension and correlation dimension are more obvious, thus information dimension and correlation dimension are selected as inpus, and the evaluation model of inter-turn short circuit position is established based on probabilistic neural network.
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Broch-Lips, Martin, Thomas Holm Pedersen, and Ole Bækgaard Nielsen. "Effect of purinergic receptor activation on Na+-K+ pump activity, excitability, and function in depolarized skeletal muscle." American Journal of Physiology-Cell Physiology 298, no. 6 (June 2010): C1438—C1444. http://dx.doi.org/10.1152/ajpcell.00361.2009.
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Activity-induced elevation of extracellular purines and pyrimidines has been associated with autocrine and paracrine signaling in many tissues. Here we investigate the effect of purinergic signaling for the excitability and contractility of depolarized skeletal muscle. Muscle excitability was experimentally depressed by elevating the extracellular K+ from 4 to 10 mM, which reduced the tetanic force to 24 ± 2% of the force at 4 mM K+. Upon addition of 1 mM ATP, however, the force recovered to 65 ± 8% of the control force ( P < 0.001, n = 5). A similar recovery was seen with ADP, but not with UTP or adenosine. The ATP-induced force recovery could be inhibited by P2Y1 receptor antagonists (3 μM SCH-202676 or 1 μM MRS-2500). A fourfold increase in M-wave area demonstrated that the ATP-induced force recovery was associated with restoration of muscle excitability ( P < 0.05, n = 4). Experiments using 86Rb+ as a tracer for K+ showed that ATP also induced a twofold increase in the activity of muscle Na+-K+ pumps. The force recovery and the stimulation of the Na+-K+ pump activity by ATP were inhibited by 50 μM of the phospholipase C inhibitor U-73122. It is concluded that purinergic signaling can increase the Na+-K+ pump activity and improve force and excitability of depolarized skeletal muscles. This novel purinergic regulation may be important for the maintenance of muscle excitability during intense exercise, where the extracellular K+ can increase substantially.