Calcium efflux and histamine secretion from rat peritoneal mast cells

Pearce, F.L.; White, John R.

doi:10.1007/bf01973835

Cited by 21 publications

(10 citation statements)

References 10 publications

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“…4), we have been able to indicate two potentially different mechanisms involved in the efflux. One of these requires the presence of sodium in the external medium and thus conforms with, although does not identify, a sodium-calcium exchanger as reported for mast and other cells [49,501. The other one is less defined as yet and appears to depend on the aggregated state of Fc,R (Fig.…”

Section: The Mechanisms Involved In the Early Calcium Signalsupporting

confidence: 78%

Activation of rat basophilic leukemia cells

Ran

Rivnay

1988

European Journal of Biochemistry

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Antigen-induced 45calcium influx into rat basophilic leukemia (RBL) cells was examined with emphasis on the early time domain under conditions that exclude loss of the cation during the subsequent washing step. Such preparations demonstrate a distinct, temporally separate influx peaking at 3 min, followed by a substantial efflux. This internalized 45Ca2 + approaches millimolar total intracellular concentration and is therefore either sequestered or becomes bound to intracellular components (proteins). The amplitude of this influx is linearly proportional to IgE-receptor occupancy at low receptor occupancies, and is sensitive to the anti-allergic drug cromolyn. Furthermore, the timing of both the maximal uptake and the maximal susceptibility to cromolyn correlates with the Quin-2 signal in these cells, and the initial degranulation pattern bears some resemblance to trends in the 45Ca2+ uptake curve. These qualities suggest that the early peak at 2-3 min, rather than any later 4 5~~2 + uptake, comprises the initial signalling Ca2+ pool. Maximal apparent inhibition by cromolyn for uptake was about 65% and required a 10-15-min preincubation with the cells. The inhibitory effect was limited to the peak at 3 min, suggesting that tracer incorporation beyond 5 -6 min largely involves other pools or pathways, triggered by receptor aggregation, yet only indirectly related to channel activity or to the signal proper. A quantitative similarity was found between the early peak measured on intact cells and the single channel conductance measured on reconstituted planar bilayers containing the purified receptor for IgE and the purified cromolyn-binding protein [Corcia, A. et al. (1986) EMBO J. 5, 849-8541. This, as well as the effects of cromolyn, support the assumption that cromolyn-binding protein is a major constituent involved in this early influx, or that influx is a principal pathway for the signaling calcium mass. membrane target protein for cromolyn and, thirdly, that the Fc,R-channel interaction is not mediated by other proteins. It also conforms with the suggestion [24] that the channel must be topologically close to the receptors for IgE in order to induce directional degranulation upon triggering of a restricted surface area of the cell (e.g. as achieved with immobilized concanavalin A). Quantitative assessment of channel activity in intact cells is difficult. On the one hand, studies with fluorescent probes do not unequivocally rule out the release of Ca2+ from intracellular pools of bound and/ or sequestered calcium, let alone the potential interference of the probe itself with the measurement. On the other hand, in as much as kinetics is concerned, studies with 45Ca2+ were inconsistent with the rise and subsequent gradual decrease in [Ca2+Ii, which form a distinct peak [16, 251. The uptake of Ca2+ was usually delayed and appeared to culminate in a plateau rather than to decrease gradually to the pretriggering level. One explanation for this may be the existence of other distinct modes of calcium incorporation th...

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Section: The Mechanisms Involved In the Early Calcium Signalsupporting

confidence: 78%

Activation of rat basophilic leukemia cells

Ran

Rivnay

1988

European Journal of Biochemistry

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“…Enhancement of histamine release from rat mast cells by PtdSer was thought to be due to an enhancement of Ca2+ influx or inhibition of Ca2+ efflux (or both) (3,4,19). Indeed, the results reported here have shown that PtdSer enhanced the stimulus-dependent increase in quin-2 signal and diminished the rate at which the quin-2 sig- (24).…”

Section: Discussionmentioning

confidence: 70%

“…Passively sensitized and quin-2-loaded mast -cells were incubated for 1 min with 50 ,ug of PtdSer per ml prior to exposure to DNP-HS albumin. The 19.3% ± 0.8% and 16.0% ± 0.5%; samples B and E, 0.5 ng/ml, 10.3% ± 0.3% and 11.6% + 2.1%; samples C and F, 0.1 ng/ml, 5.6% ± 0.6% and 7.6% ± 1.5%. results shown in Fig.…”

Section: Resultsmentioning

confidence: 94%

Direct demonstration of increased intracellular concentration of free calcium as measured by quin-2 in stimulated rat peritoneal mast cell.

White

Ishizaka²,

Sha'afi

1984

Proc. Natl. Acad. Sci. U.S.A.

109

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Rat mast cells, passively sensitized with monoclonal mouse IgE antibody, were stimulated with multivalent antigen, and an increase in cytoplasmic Ca2+ was determined by using the fluorescent probe quin-2. The increase in quin-2 fluorescence reached maximum within 20 sec after the antigen challenge and then gradually declined. A substantial increase in quin-2 fluorescence was observed in the presence of EGTA, indicating that bridging of cell-bound IgE antibody molecules by antigen induced not only Ca2' influx but also mobilization of intracellular Ca2+. Phosphatidylserine added to the medium enhanced both the antigen-induced histamine release and the increase in quin-2 fluorescence and slowed the rate at which the quin-2 signal returned to basal levels. Both the antigen-induced increase in quin-2 fluorescence and histamine release were inhibited by pretreatment of mast cells with inhibitors of methyltransferases, theophylline, or cromoglycate. It was also found that methyltransferase inhibitors and theophylline inhibited not only stimulus-dependent calcium influx but also release of bound calcium from intracellular stores. Other secretagogues, compound 48/80 (1 pg/ml) and Ca ionophore A23187 (0.1 /uM), induced a rapid increase in cytoplasmic Ca2+ in rat mast cells and subsequent histamine release. In contrast, the cocarcinogenic compound phorbol 12-myristate 13-acetate caused histamine release without increasing the quin-2 fluorescence.

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“…The main mechanism for the extrusion of calcium in this system appears to be through the operation of a sodium-calcium antiporter (Pearce & White, 1984 …”

Section: Calcium Effluxmentioning

confidence: 99%

Calcium and mast cell activation.

Pearce¹

1985

Brit J Clinical Pharma

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Calcium efflux and histamine secretion from rat peritoneal mast cells

Cited by 21 publications

References 10 publications

Activation of rat basophilic leukemia cells

Activation of rat basophilic leukemia cells

Direct demonstration of increased intracellular concentration of free calcium as measured by quin-2 in stimulated rat peritoneal mast cell.

Calcium and mast cell activation.

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