Key result
SOCE blockers reduce brain infarct size in a murine stroke model by suppressing platelet-dependent coagulation.
Why the study?
Pharmacological blockage of platelet Orai1 channels mediating SOCE may provide a novel antithrombotic therapy, but its thromboprotective effect was not determined.
Do store-operated calcium channel blockers reduce thrombus formation and brain infarct size in preclinical models?
Population
Washed human platelets, platelets from Orai1-deficient mice, and a murine stroke model
Comparison
SOCE blockers including SKF96365, 2-aminoethyl diphenylborate, MRS1845, Synta66, and GSK-7975A versus control
Design
Preclinical experimental study
Authors
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Should not change practice; hypothesis-generating for SOCE blockade in human thrombotic stroke.
Do store-operated calcium channel blockers reduce thrombus formation and brain infarct size in preclinical models?
Plasma-soluble SOCE blockers such as 2-aminoethyl diphenylborate suppress platelet-dependent coagulation and may serve as a novel target for preventing thrombotic events.
Kruchten et al. (2012) studied Thrombosis and brain infarction. Store-operated calcium channel (SOCE) blockers (e.g., 2-aminoethyl diphenylborate) was evaluated on Platelet responses, thrombus formation, and brain infarct size. Plasma-soluble SOCE blockers such as 2-aminoethyl diphenylborate suppressed platelet-dependent coagulation and markedly diminished brain infarct size in a murine stroke model.
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