Bromo-A23187: A nonfluorescent calcium ionophore for use with fluorescent probes

Deber, Charles M.; Tom-Kun, Jean; Mack, Esther; Grinstein, Sergio

doi:10.1016/0003-2697(85)90550-0

Cited by 77 publications

(28 citation statements)

References 10 publications

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“…Calibration ofthe intracellular Ca2+ signal was accomplished using an F,,, signal obtained with 30 AM Br-A23187, and Fi.... signal obtained with 0.5 mM MnC12 and Kd = 224 nM. Br-A23 187 is a nonfluorescent calcium ionophore that is also permeable to Mn2+ (14). Mn2+ is an effective quencher of fura-2 fluorescence (15).…”

Section: Methodsmentioning

confidence: 99%

Insulin attenuates vasopressin-induced calcium transients and a voltage-dependent calcium response in rat vascular smooth muscle cells.

Standley¹,

Zhang²,

Ram³

et al. 1991

J. Clin. Invest.

126

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Insulin attenuates the contractile responses of vascular smooth muscle (VSM) to various agonists. Insulinopenic and insulinresistant rats lack this normal attenuation of vascular contractile responses. To study this attenuating mechanism, the effects of insulin on calcium (Ca2") responses of cultured VSM cells (a7r5) to arginine vasopressin (AVP) and membrane potential were investigated. Insulin (1 and 100 mU/ml) shifted AVP dose-response curves to the right, reducing relative potency of AVP by 16-fold and 220-fold, respectively. Responses to AVP were significantly attenuated within 30 min of insulin application. The AVP-elicited rise in [Ca2"I] was partially dependent upon extracellular Ca2". AVP-elicited inward current was reduced by 90 min of insulin treatment (100 mU/ml), from a peak current of -103±27 pA (normal) to -37±15 pA (insulin treated). Peak voltage-dependent Ca2"-dependent inward current was unaffected by insulin; however, the current-voltage curve was shifted 16±3 mV to the right by insulin. Thus, insulin may reduce VSM contractile responses by attenuating agonistmediated rises in ICa2"I mediated, in part, by reductions in Ca2" influx through both receptor-and voltage-operated channels. (J. Clin. Invest. 1991. 88:1230-1236

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Section: Methodsmentioning

confidence: 99%

Insulin attenuates vasopressin-induced calcium transients and a voltage-dependent calcium response in rat vascular smooth muscle cells.

Standley¹,

Zhang²,

Ram³

et al. 1991

J. Clin. Invest.

126

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“…Cells were incubated in the presence or absence of a variety of potential modulators of apoptosis. These included the calcium ionophores A23187, 4-bromo-A23187 (19), and ionomycin; the calmodulin antagonist W-7 [N(6-aminohexyl)-5-chloro-l-naphthalene sulfonamide, HC1] (20) and BAPTA/AM, which chelates intracellular calcium (21 ). Stock solutions of W-7 were prepared in methanol (final concentration of methanol 0.05%, vol/ vol).…”

Section: Introductionmentioning

confidence: 99%

Transient elevations of cytosolic free calcium retard subsequent apoptosis in neutrophils in vitro.

Whyte¹,

Hardwick²,

Meagher³

et al. 1993

J. Clin. Invest.

139

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Elevation of cytosolic calcium (ICa2+I;) has been reported to induce apoptosis in a number of cell types. However, in the neutrophil, which undergoes apoptosis constitutively during aging in vitro, activation by inflammatory mediators elevates ICa2Ji; and prolongs lifespan via inhibition of apoptosis. To examine this paradox, we investigated the effects of modulation of [Ca2" I upon apoptosis of neutrophils in vitro. Calcium ionophores (A23187, ionomycin) retarded apoptosis in neutrophil populations after 20 h (P < 0.001). Conversely, intracellular Ca2+-chelation, using bis-(o-aminophenoxy)-NNNN'-tetraacetic acid (BAPTA) acetoxymethyl ester (AM) promoted apoptosis (P < 0.02). W-7 (an inhibitor of calmodulin) also promoted apoptosis (P < 0.05). Measurements of ICa2+I,, using fura-2, showed (a) increased apoptosis in neutrophil populations was not associated with elevated ICa2I]1, (b) neutrophils cultured with ionophore at concentrations inhibiting apoptosis exhibited transient ( < 1 h) elevations of[Ca2Ijl, to levels previously reported with receptor-mediated stimuli, and (c) BAPTA was able to prevent the elevation of ICa2+Ij and the inhibition of apoptosis produced by ionophore. Modulation of apoptosis occurred without alterations in intracellular pH. Thus, in the neutrophil, unlike lymphoid cells, elevation of ICa2+Ii exerts an inhibitory effect upon apoptosis. Furthermore, these data suggest that transient elevation of ICa2"I elicits signaling events leading to prolonged inhibition of apoptosis. (J. Clin. Invest. 1993. 92:446-455.)

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“…After the loading period, the cells were washed with 15 ml of the extracellular bath solution to remove any excess dye not taken up by the cells. To determine the proportion of loaded Fura-2AM that had been converted to the free acid and that was accessible to calcium entering from the external solution, cells loaded with Fura-2AM were exposed to 1-10 #sm-4Br-A23187 (Deber, Tom-Kun, Mack & Grinstein, 1985) and then to 2-5 mm-external Mn21. As with Quin-2 (Hesketh, Smith, Moore, Taylor & Metcalfe, 1983;Grynkiewicz et al 198,5), Mn21 binds to de-esterified Fura-2 and quenches the fluorescence.…”

Section: Fura-2 Measurementsmentioning

confidence: 99%

Calcium influx and calcium current in single synaptic terminals of goldfish retinal bipolar neurons.

Heidelberger

Matthews

1992

The Journal of Physiology

217

185

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Bromo-A23187: A nonfluorescent calcium ionophore for use with fluorescent probes

Cited by 77 publications

References 10 publications

Insulin attenuates vasopressin-induced calcium transients and a voltage-dependent calcium response in rat vascular smooth muscle cells.

Insulin attenuates vasopressin-induced calcium transients and a voltage-dependent calcium response in rat vascular smooth muscle cells.

Transient elevations of cytosolic free calcium retard subsequent apoptosis in neutrophils in vitro.

Calcium influx and calcium current in single synaptic terminals of goldfish retinal bipolar neurons.

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