ATP‐activated Ca<sup>2+</sup>‐permeable channels in rat peritoneal macrophages

Naumov, A. P.; Kuryshev, Yuri A.; Kaznacheyeva, Еlena; Mozhayeva, G. N.

doi:10.1016/0014-5793(92)81210-d

Cited by 22 publications

(17 citation statements)

References 9 publications

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“…The absence of voltage-dependent channels is not surprising given that myeloid DC, like other leukocytes, are essentially nonexcitable, and voltage-gated Ca 2ϩ channels have not been clearly demonstrated in leukocytes (4). In contrast, ATP-gated cation channels are expressed in macrophages (closely related myeloid-lineage cells) (21), mast cells (33), and T cells (22)(23)(24). ATPgated channels are Ca 2ϩ permeable.…”

Section: Discussionmentioning

confidence: 99%

Fundamental Ca2+ Signaling Mechanisms in Mouse Dendritic Cells: CRAC Is the Major Ca2+ Entry Pathway

Hsu

O’Connell

Klyachko

et al. 2001

The Journal of Immunology

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Although Ca2+-signaling processes are thought to underlie many dendritic cell (DC) functions, the Ca2+ entry pathways are unknown. Therefore, we investigated Ca2+-signaling in mouse myeloid DC using Ca2+ imaging and electrophysiological techniques. Neither Ca2+ currents nor changes in intracellular Ca2+ were detected following membrane depolarization, ruling out the presence of functional voltage-dependent Ca2+ channels. ATP, a purinergic receptor ligand, and 1–4 dihydropyridines, previously suggested to activate a plasma membrane Ca2+ channel in human myeloid DC, both elicited Ca2+ rises in murine DC. However, in this study these responses were found to be due to mobilization from intracellular stores rather than by Ca2+ entry. In contrast, Ca2+ influx was activated by depletion of intracellular Ca2+ stores with thapsigargin, or inositol trisphosphate. This Ca2+ influx was enhanced by membrane hyperpolarization, inhibited by SKF 96365, and exhibited a cation permeability similar to the Ca2+ release-activated Ca2+ channel (CRAC) found in T lymphocytes. Furthermore, ATP, a putative DC chemotactic and maturation factor, induced a delayed Ca2+ entry with a voltage dependence similar to CRAC. Moreover, the level of phenotypic DC maturation was correlated with the extracellular Ca2+ concentration and enhanced by thapsigargin treatment. These results suggest that CRAC is a major pathway for Ca2+ entry in mouse myeloid DC and support the proposal that CRAC participates in DC maturation and migration.

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Section: Discussionmentioning

confidence: 99%

Fundamental Ca2+ Signaling Mechanisms in Mouse Dendritic Cells: CRAC Is the Major Ca2+ Entry Pathway

Hsu

O’Connell

Klyachko

et al. 2001

The Journal of Immunology

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“…In view of the monocytic origin of microglia it is interesting to note that ATP is able to permeabilize to cations the plasma membranes of rat (Naumov et al, 1992) and mouse peritoneal macrophages (Steinberg et al, 1987), and of the murine macrophage-like cell-line J774 (Sung et al, 1985;Steinberg et al, 1987). This effect is associated with depolarization (Sung et al, 1985;Buisman et al, 1988) and an increase in membrane conductance (Buisman et al, 1988).…”

Section: Resultsmentioning

confidence: 99%

Characterization and possible function of adenosine 5′‐triphosphate receptors in activated rat microglia

Nörenberg

Langosch

Gebicke‐Haerter

et al. 1994

British J Pharmacology

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1 Purinoceptor agonist-induced currents in untreated (proliferating) and lipopolysaccharide (LPS; 100 ng ml`)-treated (non-proliferating) rat microglial cells in culture were recorded by the whole-cell patch-clamp technique. These cells have two preferred resting membrane potentials, one at -35 mV and another one at -70 mV. 2 Most experiments were carried out in non-proliferating cells. ATP, ATP--y-S and X,4-MeATP (1 -1000 jLM in all cases) evoked an inward current at a holding potential of -70 mV, followed, in some experiments, by an outward current. At -70 mV 2-methylthio ATP (1-1I000 1M) evoked an inward current, whereas at -35 mV it produced an outward current only. 3 When K+ was replaced in the pipette solution by an equimolar concentration of Cs' (150 mM), the main outward component of the ATP-y-S (10 LM) induced response disappeared. Instead, an inward current was obtained. Replacement of K+ by Cs' did not affect the inward current evoked by 2-methylthio ATP (300 pM). 4-Aminopyridine (1-1O mM), however, almost abolished this current and unmasked a smaller outward current.4 The rank order of agonist potency was 2-methylthio ATP > ATP> aP-MeATP. Adenosine and UTP were inactive. Suramin (300 JLM) and reactive blue 2 (50 gLM) antagonized the effect of 2-methylthio ATP (300 tiM). 5I-V relations were determined by delivering fast voltage ramps before and during the application of 2-methylthio ATP (300 JAM). In the presence of extra-(1 mM) and intracellular (150 mM) Cs', the 2-methylthio ATP-evoked current crossed the zero current level near 0 mV. When both Cs' (1 mm) and 4-aminopyridine (1 mM) were present in the bath medium, the intersection of the 2-methylthio ATP current with the zero current level was near -75 mV. 6 2-Methylthio ATP (1-1I000 jM) induced the same inward current both in proliferating and nonproliferating microglia. However, the depolarizing response to 2-methylthio ATP (300 laM) was larger and longer-lasting in the proliferating cells. When the free Ca2" concentration in the pipettes was increased from the standard 0.01 to 1 JAM, the amplitude and duration of this depolarization was increased in non-proliferating cells. 4-Aminopyridine (1 mM) enhanced the duration, but not the amplitude of responses.7 ATP and its structural analogues stimulate microglial purinoceptors of the P2Y-type. This leads to the opening of non-selective cationic channels and potassium channels. Depending on the resting membrane potential, depolarization or hyperpolarization prevails. Although the inward current produced by 2-methylthio ATP is of similar amplitude in proliferating and non-proliferating microglia, the resulting depolarization is smaller in the latter cell type because of the presence of voltage-sensitive, outwardly rectifying potassium channels.

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“…Hence, these channels can be referred to as G protein-gated channels (Yatani et al 1987a) in contrast to the channels that are merely regulated by G proteins (Holz, Rane & Dunlap, 1986;Yatani et al 1987 b;Dolphin, Scott & Wooton, 1988;Schubert, VanDongen, Kirsh & Brown, 1989;Mathie, Bernheim & Hille, 1992). The G protein-gated Ca2P-permeable channels dependent on activation of the epidermal growth factor receptor have been characterized in our previous studies on A431 cells (Mozhayeva et al 1991;Naumov et al 1993;Kuryshev et al 1993 (Naumov et at. 1992) are identical to those activated under normal conditions by ATP bound to the receptor.…”

Section: Discussionmentioning

confidence: 99%

ATP‐operated calcium‐permeable channels activated via a guanine nucleotide‐dependent mechanism in rat macrophages.

Naumov

Kiselyov

Mamin

et al. 1995

The Journal of Physiology

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ATP‐activated Ca²⁺‐permeable channels in rat peritoneal macrophages

Cited by 22 publications

References 9 publications

Fundamental Ca2+ Signaling Mechanisms in Mouse Dendritic Cells: CRAC Is the Major Ca2+ Entry Pathway

Fundamental Ca2+ Signaling Mechanisms in Mouse Dendritic Cells: CRAC Is the Major Ca2+ Entry Pathway

Characterization and possible function of adenosine 5′‐triphosphate receptors in activated rat microglia

ATP‐operated calcium‐permeable channels activated via a guanine nucleotide‐dependent mechanism in rat macrophages.

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ATP‐activated Ca2+‐permeable channels in rat peritoneal macrophages

Cited by 22 publications

References 9 publications

Fundamental Ca2+ Signaling Mechanisms in Mouse Dendritic Cells: CRAC Is the Major Ca2+ Entry Pathway

Fundamental Ca2+ Signaling Mechanisms in Mouse Dendritic Cells: CRAC Is the Major Ca2+ Entry Pathway

Characterization and possible function of adenosine 5′‐triphosphate receptors in activated rat microglia

ATP‐operated calcium‐permeable channels activated via a guanine nucleotide‐dependent mechanism in rat macrophages.

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ATP‐activated Ca²⁺‐permeable channels in rat peritoneal macrophages