14,15-cis-episulfide-eicosatrienoic acid, an 'Epoxygenase' eicosanoid analog, inhibits ionophore- but not thrombin-induced platelet aggregation

K. Bernstrom; K. Malcolm; J. Mcgee; J. Maclouf; S. Levy-Toledano; J R Falck; F. A. Fitzpatrick

14,15-cis-episulfide-eicosatrienoic acid, an 'Epoxygenase' eicosanoid analog, inhibits ionophore- but not thrombin-induced platelet aggregation

K. Bernstrom, K. Malcolm, J. Mcgee, J. Maclouf, S. Levy-Toledano, J R Falck, F. A. Fitzpatrick

Biochemistry

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

An 'epoxygenase' eicosanoid analog, 14,15-cis-episulfide-eicosatrienoic acid, has several unique pharmacological effects on platelets. These include (i) inhibition of ionophore A23187- but not thrombin-induced activation, (ii) inhibition of thromboxane B₂ biosynthesis derived from endogenous but not exogenous arachidonic acid, and (iii) attenuation of ionophore-mediated increases in cytosolic Ca²⁺ when extracellular or membrane Ca²⁺ is available but not when these pools are excluded. Neither elevation of cyclic AMP levels, a potent inhibitory process, nor direct antagonism of the prostaglandin H₂/thromboxane A₂ receptor is responsible for the actions of 14,15-cis-episulfide- eicosatrienoic acid. These properties distinguish 14,15-cis-episulfide-eicosatrienoic acid from other antiaggregatory substances.

Original language	English (US)
Pages (from-to)	114-119
Number of pages	6
Journal	Molecular Pharmacology
Volume	39
Issue number	2
State	Published - Feb 1991

ASJC Scopus subject areas

Molecular Medicine
Pharmacology

Cite this

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title = "14,15-cis-episulfide-eicosatrienoic acid, an 'Epoxygenase' eicosanoid analog, inhibits ionophore- but not thrombin-induced platelet aggregation",

abstract = "An 'epoxygenase' eicosanoid analog, 14,15-cis-episulfide-eicosatrienoic acid, has several unique pharmacological effects on platelets. These include (i) inhibition of ionophore A23187- but not thrombin-induced activation, (ii) inhibition of thromboxane B2 biosynthesis derived from endogenous but not exogenous arachidonic acid, and (iii) attenuation of ionophore-mediated increases in cytosolic Ca2+ when extracellular or membrane Ca2+ is available but not when these pools are excluded. Neither elevation of cyclic AMP levels, a potent inhibitory process, nor direct antagonism of the prostaglandin H2/thromboxane A2 receptor is responsible for the actions of 14,15-cis-episulfide- eicosatrienoic acid. These properties distinguish 14,15-cis-episulfide-eicosatrienoic acid from other antiaggregatory substances.",

author = "K. Bernstrom and K. Malcolm and J. Mcgee and J. Maclouf and S. Levy-Toledano and Falck, {J R} and Fitzpatrick, {F. A.}",

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T1 - 14,15-cis-episulfide-eicosatrienoic acid, an 'Epoxygenase' eicosanoid analog, inhibits ionophore- but not thrombin-induced platelet aggregation

AU - Bernstrom, K.

AU - Malcolm, K.

AU - Mcgee, J.

AU - Maclouf, J.

AU - Levy-Toledano, S.

AU - Falck, J R

AU - Fitzpatrick, F. A.

PY - 1991/2

Y1 - 1991/2

N2 - An 'epoxygenase' eicosanoid analog, 14,15-cis-episulfide-eicosatrienoic acid, has several unique pharmacological effects on platelets. These include (i) inhibition of ionophore A23187- but not thrombin-induced activation, (ii) inhibition of thromboxane B2 biosynthesis derived from endogenous but not exogenous arachidonic acid, and (iii) attenuation of ionophore-mediated increases in cytosolic Ca2+ when extracellular or membrane Ca2+ is available but not when these pools are excluded. Neither elevation of cyclic AMP levels, a potent inhibitory process, nor direct antagonism of the prostaglandin H2/thromboxane A2 receptor is responsible for the actions of 14,15-cis-episulfide- eicosatrienoic acid. These properties distinguish 14,15-cis-episulfide-eicosatrienoic acid from other antiaggregatory substances.

AB - An 'epoxygenase' eicosanoid analog, 14,15-cis-episulfide-eicosatrienoic acid, has several unique pharmacological effects on platelets. These include (i) inhibition of ionophore A23187- but not thrombin-induced activation, (ii) inhibition of thromboxane B2 biosynthesis derived from endogenous but not exogenous arachidonic acid, and (iii) attenuation of ionophore-mediated increases in cytosolic Ca2+ when extracellular or membrane Ca2+ is available but not when these pools are excluded. Neither elevation of cyclic AMP levels, a potent inhibitory process, nor direct antagonism of the prostaglandin H2/thromboxane A2 receptor is responsible for the actions of 14,15-cis-episulfide- eicosatrienoic acid. These properties distinguish 14,15-cis-episulfide-eicosatrienoic acid from other antiaggregatory substances.

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ER -

14,15-cis-episulfide-eicosatrienoic acid, an 'Epoxygenase' eicosanoid analog, inhibits ionophore- but not thrombin-induced platelet aggregation

Abstract

ASJC Scopus subject areas

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