Evaluation of platelet calcium ion mobilization by the use of various divalent ions

Yukio, Ozaki; Yatomi, Yutaka; Kudoh, Shoji

doi:10.1016/0143-4160(92)90026-o

Cited by 29 publications

(22 citation statements)

References 12 publications

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“…5C). Since Ba2P is known to permeate InsP3 receptors (Bezprozvanny & Ehrlich, 1993) (Ozaki, Yatomi & Kume, 1992;Jenner, Farndale & Sage, 1994). While our work was in progress, another report of AVP effects on bivalent cation fluxes in A7r5 cells appeared (Hughes & Schachter, 1994).…”

Section: Discussionmentioning

confidence: 99%

Vasopressin stimulation of Ca2+ mobilization, two bivalent cation entry pathways and Ca2+ efflux in A7r5 rat smooth muscle cells.

Byron

Taylor

1995

The Journal of Physiology

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Section: Discussionmentioning

confidence: 99%

Vasopressin stimulation of Ca2+ mobilization, two bivalent cation entry pathways and Ca2+ efflux in A7r5 rat smooth muscle cells.

Byron

Taylor

1995

The Journal of Physiology

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“…To assess basal Ca 2+ channel activity without agonist stimulation, Ba 2+ was added to platelets in Ca 2+ ‐free medium to act as a calcium surrogate. Ba 2+ enters the cell through Ca 2+ channels, but unlike Ca 2+ , it cannot be extruded from the cell by plasma membrane Ca 2+ ‐ATPase pump therefore it accumulates in the cell (Ozaki et al ., 1992; Zschauer et al ., 1988; Blache & Clavatti, 1987; Blache et al ., 1987). The removal of Ba 2+ from the cytoplasm by the endoplasmic reticulum may be limited when compared to Ca 2+ and Sr 2+ (Ozaki et al ., 1992).…”

Section: Methodsmentioning

confidence: 99%

trans‐Resveratrol inhibits calcium influx in thrombin‐stimulated human platelets

Dobrydneva

Williams

Blackmore

1999

British J Pharmacology

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1 The phytoestrogenic compound trans-resveratrol (trans-3,5,4'-trihydroxystilbene) is found in appreciable quantities in grape skins and wine. It has been shown that both products rich in transresveratrol and pure trans-resveratrol inhibit platelet aggregation both in vivo and in vitro. However the mechanism of this action still remains unknown. 2 An essential component of the aggregation process in platelets is an increase in intracellular free Ca 2+ ([Ca 2+ ] i ). Ca 2+ must enter the cell from the external media through speci®c and tightly regulated Ca 2+ channels in the plasma membrane. The objective of this study was to characterize what e ect trans-resveratrol had on the Ca 2+ channels in thrombin stimulated platelets. 3 In this study we showed that trans-resveratrol immediately inhibited Ca 2+ in¯ux in thrombinstimulated platelets with an IC 50 of 0.5 mM. trans-Resveratrol at 0.1, 1.0 and 10.0 mM produced 20+6, 37+6 and 57+4% inhibition respectively of the e ect of thrombin (0.01 u ml 71 ) to increase [Ca 2+ ] i . 4 trans-Resveratrol also inhibited spontaneous Ba 2+ entry into Fura-2 loaded platelets, with 0.1, 1.0 and 10.0 mM trans-resveratrol producing 10+5, 30+5 and 50+7% inhibition respectively. This indicated that trans-resveratrol directly inhibited Ca 2+ channel activity in the platelets in the absence of agonist stimulation. 5 trans-Resveratrol also inhibited thapsigargin-mediated Ca 2+ in¯ux into platelets. This suggests that the store-operated Ca 2+ channels are one of the possible targets of trans-resveratrol. These channels rely on the emptying of the internal Ca 2+ stores to initiate in¯ux of Ca 2+ into the cell. 6 The phytoestrogens genistein, daidzein, apigenin and genistein-glucoside (genistin) produced inhibitory e ects against thrombin similar to those seen with trans-resveratrol. 7 We conclude that trans-resveratrol is an inhibitor of store-operated Ca 2+ channels in human platelets. This accounts for the ability of trans-resveratrol to inhibit platelet aggregation induced by thrombin.

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“…Traces a, algC alone; b, 1 k g . [Ozaki et al, 1992;Premack et al, 19941. However, the ability of this cation to pass through a Ca2+ transporter, such as a carrier, exchanger, or pump in the cell membrane, is extremely limited [Ozaki et al, 1992;Premack et al, 19941.…”

Section: Cross-linking Of Cd3 Molecules Induced a Biphasic Rise Of [Cmentioning

confidence: 97%

“…[Ozaki et al, 1992;Premack et al, 19941. However, the ability of this cation to pass through a Ca2+ transporter, such as a carrier, exchanger, or pump in the cell membrane, is extremely limited [Ozaki et al, 1992;Premack et al, 19941. As a result, increased Fura-2 fluorescence induced by the entry of divalent cation is sustained for a relatively longer period of time with Ba2+ than with Ca2+.…”

Section: Cross-linking Of Cd3 Molecules Induced a Biphasic Rise Of [Cmentioning

confidence: 97%

T cell receptor‐mediated Ca²⁺ signaling: Release and influx are independent events linked to different Ca²⁺ entry pathways in the plasma membrane

Chakrabarti

Chang

Erickson

1995

J of Cellular Biochemistry

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In this study, we showed that cross-linking CD3 molecules on the T cell surface resulted in Ca2+ release from the intracellular stores followed by a sustained Ca2+ influx. Inhibition of release with TMB-8 did not block the influx. However, inhibition of phospholipase C activity suppressed both Ca2+ release and influx. Once activated, the influx pathway remained open in the absence of further hydrolysis of PIP2. Thapsigargin, a microsomal Ca(2+)-ATPase inhibitor, stimulated Ca2+ entry into the cells by a mechanism other than emptying Ca2+ stores. In addition, Ca2+ entry into the Ca(2+)-depleted cells was stimulated by low basal level of cytosolic Ca2+, not by the emptying of intracellular Ca2+ stores. Both the Ca2+ release and influx were dependent on high and low concentrations of extracellular Ca2+. At low concentrations, Mn2+ entered the cell through the Ca2+ influx pathway and quenched the sustained phase of fluorescence; whereas, at higher Mn2+ concentration both the transient and the sustained phases of fluorescence were quenched. Moreover, Ca2+ release was inhibited by low concentrations of Ni2+, La3+, and EGTA, while Ca2+ influx was inhibited by high concentrations. Thus, in T cells Ca2+ influx occurs independently of IP3-dependent Ca2+ release. However, some other PIP2 hydrolysis-dependent event was involved in prolonged activation of Ca2+ influx. Extracellular Ca2+ influenced Ca2+ release and influx through the action of two plasma membrane Ca2+ entry pathways with different pharmacological and biochemical properties.

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Evaluation of platelet calcium ion mobilization by the use of various divalent ions

Cited by 29 publications

References 12 publications

Vasopressin stimulation of Ca2+ mobilization, two bivalent cation entry pathways and Ca2+ efflux in A7r5 rat smooth muscle cells.

Vasopressin stimulation of Ca2+ mobilization, two bivalent cation entry pathways and Ca2+ efflux in A7r5 rat smooth muscle cells.

trans‐Resveratrol inhibits calcium influx in thrombin‐stimulated human platelets

T cell receptor‐mediated Ca²⁺ signaling: Release and influx are independent events linked to different Ca²⁺ entry pathways in the plasma membrane

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Evaluation of platelet calcium ion mobilization by the use of various divalent ions

Cited by 29 publications

References 12 publications

Vasopressin stimulation of Ca2+ mobilization, two bivalent cation entry pathways and Ca2+ efflux in A7r5 rat smooth muscle cells.

Vasopressin stimulation of Ca2+ mobilization, two bivalent cation entry pathways and Ca2+ efflux in A7r5 rat smooth muscle cells.

trans‐Resveratrol inhibits calcium influx in thrombin‐stimulated human platelets

T cell receptor‐mediated Ca2+ signaling: Release and influx are independent events linked to different Ca2+ entry pathways in the plasma membrane

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T cell receptor‐mediated Ca²⁺ signaling: Release and influx are independent events linked to different Ca²⁺ entry pathways in the plasma membrane