The Signal for Capacitative Calcium Entry

Putney, James W.

doi:10.1007/978-1-4684-6471-9_3

Cited by 113 publications

(148 citation statements)

References 195 publications

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“…Our own observations, and those of other groups [35][36][37], demonstrate that this store of Ca 2 contributes only a small fraction to the initial Ca 2 elevation. Several investigators have tried to identify the pathway that initiates Ca 2 influx across the plasma membrane [18][19][20][21][22], but the exact mechanism remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Characterization of altered calcium signalling in T lymphocytes from patients with rheumatoid arthritis (RA)

Carruthers

Naylor

Allen

et al. 1996

Clinical and Experimental Immunology

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SUMMARYAbnormal function of peripheral blood T lymphocytes is characteristic of RA; diminished proliferation and secretion of cytokines following in vitro mitogen stimulation are observed. We have investigated the calcium flux initiating T cell activation in rheumatoid peripheral blood mononuclear cells (PBMC) to determine whether abnormalities in signalling are also present. We have found that both phytohaemagglutinin (PHA-P)-and anti-CD3-stimulated calcium fluxes were much reduced in the patients' PBMC compared with controls, with a mean six-fold difference (P < 0 . 01) in rate of Ca 2 flux with PHA-P stimulation. When purified T cells were examined with PHA and CD3 stimulation, a reduction in the peak and plateau [Ca 2 ] i was observed in RA T cells, but the rate of rise of [Ca 2 ] i was only reduced in those cells stimulated with PHA. These results suggest that alterations in the initiating signal may underlie the functional T cell abnormalities associated with RA, and that there may be an additional extrinsic influence from non-T cells in the PBMC population.

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Section: Discussionmentioning

confidence: 99%

Characterization of altered calcium signalling in T lymphocytes from patients with rheumatoid arthritis (RA)

Carruthers

Naylor

Allen

et al. 1996

Clinical and Experimental Immunology

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“…Further, voltage-operated Ca2"-channels are apparently not involved in the activation of nAChR-mediated Ca2"-entry for the sustained phase of the Ca2+ response was unaffected by diltiazem or by depolarization of the cells. It is also unlikely that the nAChR-evoked Ca2+-entry is dependent on the filling state of the Ca21 stores (Putney & Bird, 1993;Randriamampita & Tsien, 1993), because Ca2+-entry was still observed under conditions blocking Ca2" mobilization such as low external Na+ or high K+. Finally, the nAChR-mediated Ca2"-entry in C2C12 cells was not affected by La3+, which supports the idea that a process is involved which differs from Ca2+-entry induced by stimulation of G-protein coupled receptors activating phospholipase C Henning et al, 1993a).…”

Section: Discussionmentioning

confidence: 99%

“…The absence of the sustained phase in the presence of high K+ or carbachol suggests that the mechanism responsible for P2u-purinoceptor-induced Ca2 +-entry is dependent on the electro-chemical gradient and therefore voltage-dependent. Capacitive Ca2+-entry, following emptying of Ins(1,4,5)P3 sensitive stores (Putney & Bird, 1993;Randriamampita & Tsien, 1993), has not been observed in C2C12 myotubes (Henning, unpublished). Thus the mechanism leading to Ca2+-entry on P2u-purinoceptor is unknown.…”

Section: P2-purinoceptor-mediated Ca2+ Responsementioning

confidence: 99%

Different mechanisms of Ca²⁺‐handling following nicotinic acetylcholine receptor stimulation, P_2U‐purinoceptor stimulation and K⁺‐induced depolarization in C2C12 myotubes

Henning

Duin

Popta

et al. 1996

British J Pharmacology

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1 The increase in intracellular Ca2+ on nicotinic acetylcholine receptor (nAChR) stimulation, P2U-purinoceptor stimulation and K+-induced depolarization was investigated in mouse C2C12 myotubes by use of fura-2 fluorescence to characterize the intracellular organisation of Ca2+ releasing stores and Ca2+ -entry process.2 Stimulation of nAChRs with carbachol induced a rapid rise in internal Ca2+ (EC50 = 0.85 + 0.09 gM), followed by a sustained phase. The Ca2+ response evoked by carbachol (10 gM) was completely blocked by the nAChR antagonist, pancuronium (3 gM), but was not affected by the muscarinic antagonist, atropine (3 gM), or under conditions when Ca2+ entry was blocked by La3`(50 gM) or diltiazem (10 gM). Addition of pancuronium (3 gM) during the sustained phase of the carbachol-evoked response did not affect this phase.3 Stimulation of P2U purinoceptors with ATP (1 mM) induced a somewhat higher biphasic Ca2+ response (EC50 of the rapid phase: 8.72+0.08 gM) than with carbachol. Pretreatment with La3+ abolished the sustained phase of the ATP-induced Ca2+ response, while the response was unaffected by diltiazem or pancuronium. 4 Stimulation of the cells with high K+ (60 mM), producing the same depolarization as with carbachol (10 gM), induced a rapid monophasic Ca2`response, insensitive to diltiazem, pancuronium or La3 .5 Under Ca2+ -free conditions, the sustained phase of the carbachol-and ATP-evoked responses were abolished. Pre-emptying of depolarization-sensitive stores by high K+ under Ca2+-free conditions did not affect the carbachol-or ATP-evoked Ca2+ mobilization and vice versa. Preincubation of the cells with ATP in the absence of extracellular Ca2+ decreased the amplitude of the subsequent carbacholinduced Ca2+ response to 11 %, while in the reverse procedure the ATP-induced response was decreased to 65%. Ca2+ mobilization evoked by simultaneous addition of optimal concentrations of carbachol and ATP was increased compared to levels obtained with either agonist. 6 Preincubation with high K+ under normal conditions abolished the sustained phase of the ATPevoked Ca2+ response. The carbachol response consisted only of the sustained phase in the presence of high K+.7 The carbachol-induced Ca2+ response was completely abolished under low Na+/Ca2+ -free conditions, while under low Na+ conditions only a sustained Ca2+ response was observed. The ATPand K+-induced responses were changed compared to Ca2+-free conditions. 8 ATP (300 gM) induced the formation of Ins(1,4,5)P3 under Ca2+-free conditions with a comparable time course to that found for the rise in internal Ca2 . In contrast to ATP, carbachol (10 gM) did not affect Ins(1,4,5)P3 levels under Ca2+-free conditions. 9 It is concluded that the Ca2+ release from discrete stores of C2C12 myotubes is induced by stimulation of nAChRs, P2U-purinoceptors and by high K+. Only the P2U-purinoceptor and nAChR activated stores show considerable overlap in releasable Ca2. Sustained Ca2+-entry is activated by stimulation of nAChRs and P2u-purinoceptors via separate i...

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“…This dynamic process occurs during the co-ordinated events of cell shape change, spreading, adhesion, growth and migration, events which require modulation of the cytoskeleton (Burridge et al, 1992;Schaller and Parsons, 1993). The regulatory role of intracellular Ca 21 in this pathway has not been defined previously.Increase in intracellular Ca 21 concentration may be accomplished through 2 mechanisms: release from internal stores or influx across the plasma membrane (Felder et al, 1994;Putney and Bird, 1993). The selected effects of increasing intracellular Ca 21 from either mechanism have not been defined in the process of cell spreading and cell shape remodeling.…”

mentioning

confidence: 99%

“…Increase in intracellular Ca 21 concentration may be accomplished through 2 mechanisms: release from internal stores or influx across the plasma membrane (Felder et al, 1994;Putney and Bird, 1993). The selected effects of increasing intracellular Ca 21 from either mechanism have not been defined in the process of cell spreading and cell shape remodeling.…”

mentioning

confidence: 99%

Regulation of cell spreading during differentiation in the muscarinic M5 receptor tumor-suppressor model

et al. 1997

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Activation of the muscarinic receptor in Chinese hamster ovary (CHO) cells results in a reversal of the malignant phenotype for which spreading into a bipolar, fibroblastic morphology is a marker. The process of morphologic change requires multiple events, including alterations in adhesions to substrates and cytoskeletal re-arrangement. In this report, we demonstrate the calcium-dependent involvement of p125 FAK in this cellular shape change using an inhibitor of ligand-induced calcium influx, carboxyamido-triazole (CAI). p125 FAK becomes tyrosine-phosphorylated after exposure to the agonist carbachol (CC), reaching maximal phosphorylation prior to initiation of cellular shape change at 1 hr into CC exposure (386 6 103%). Phosphorylation remained elevated through the shape change (4-12 hr The Chinese hamster ovary (CHO) m5 muscarinic acetylcholine receptor (m5AChR) tumor-suppressor model is a unique model in which to study spreading-related signal-transduction events . CHO cells stably transfected with m5AChR undergo a morphologic change from stellate to fibroblastic when stimulated with the specific muscarinic agonist carbachol (CC). This shape change is associated with a marked reduction in the ability of CHOm5 cells to form tumors in nude mice . The m5AChR is coupled to multiple signal-transduction pathways, including membrane-associated phospholipases (C-b, C-g, A2 and D), release of internal Ca 21 stores, stimulation of Ca 21 influx through receptor-operated Ca 21 channels and activation of adenylyl cyclase (Felder, 1995;Felder et al., 1993;Gusovsky et al., 1993). The shape change was shown to be dependent upon m5AChR-mediated mobilization of intracellular Ca 21 or cAMP (Felder et al., , 1994Singer-Lahat et al., 1996). We have shown that this calcium influx can be inhibited by concomitant exposure to carboxyamido-triazole (CAI), an inhibitor of nonvoltage-gated calcium influx, at CAI concentrations that inhibit migration, proliferation and angiogenesis (Felder et al., 1991Kohn et al., 1994aKohn et al., , 1995. CAI blockade of CC-mediated calcium influx prevented the phenotypic change of CHOm5 cells . This spreading during the shape change provides a unique model in which to investigate the temporal nature and Ca 21 sensitivity of the signaling events underlying this tumor-suppression model.Cells interact with their extracellular environment, the extracellular matrix and basement membrane, through cell-surface contacts termed focal adhesions. Focal-adhesion contacts contain regions of enhanced tyrosine phosphorylation through which cytoskeletal elements may couple to membrane-associated signal-transducing pathways (Hansen et al., 1994;Maher et al., 1985). These points of contact are regulated in a complex fashion involving cell interaction with the extracellular substratum and subsequent outside-in signaling to direct cellular re-organization. Down-stream effector events are also complex, involving several signaling cascades, such as mobilization of intracellular Ca 21 , phosphorylation and generation of leu...

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The Signal for Capacitative Calcium Entry

Cited by 113 publications

References 195 publications

Characterization of altered calcium signalling in T lymphocytes from patients with rheumatoid arthritis (RA)

Characterization of altered calcium signalling in T lymphocytes from patients with rheumatoid arthritis (RA)

Different mechanisms of Ca²⁺‐handling following nicotinic acetylcholine receptor stimulation, P_2U‐purinoceptor stimulation and K⁺‐induced depolarization in C2C12 myotubes

Regulation of cell spreading during differentiation in the muscarinic M5 receptor tumor-suppressor model

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The Signal for Capacitative Calcium Entry

Cited by 113 publications

References 195 publications

Characterization of altered calcium signalling in T lymphocytes from patients with rheumatoid arthritis (RA)

Characterization of altered calcium signalling in T lymphocytes from patients with rheumatoid arthritis (RA)

Different mechanisms of Ca2+‐handling following nicotinic acetylcholine receptor stimulation, P2U‐purinoceptor stimulation and K+‐induced depolarization in C2C12 myotubes

Regulation of cell spreading during differentiation in the muscarinic M5 receptor tumor-suppressor model

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Different mechanisms of Ca²⁺‐handling following nicotinic acetylcholine receptor stimulation, P_2U‐purinoceptor stimulation and K⁺‐induced depolarization in C2C12 myotubes