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The membrane potential modulates thrombin-stimulated Ca²⁺ mobilization and platelet aggregation.

Abstract：

:G protein-coupled receptors can be directly modulated by changes in transmembrane voltage in a variety of cell types. Here we show that, while changes in the membrane voltage itself do not induce detectable modifications in the cytosolic Ca(2+) concentration, platelet stimulation with thrombin or the PAR-1 and PAR-4 agonist peptides SFLLRN and AYPGKF, respectively, results in Ca(2+) release from intracellular stores that is sensitive to the membrane depolarisation. Direct activation of G proteins or phospholipase C by AlF4(-) and m-3M3FBS, respectively, leads to Ca(2+) release that is insensitive to changes in the membrane potential. Thapsigargin-, as well as OAG-induced Ca(2+) entry are affected by the membrane voltage, probably as a result of the modification in the driving force for Ca(2+) influx; however, hyperpolarisation does not enhance thrombin- or OAG-evoked Ca(2+) entry probably revealing the presence of a voltage-sensitive regulatory mechanism. Transmembrane voltage also modulates the activity of the plasma membrane Ca(2+)-ATPase (PMCA) most likely due to a decrease in the phosphotyrosine content of the pump. Thrombin-stimulated platelet aggregation is modulated by membrane depolarisation by a mechanism that is, at least partially, independent of Ca(2+). These observations indicate that PAR-1 and PAR-4 receptors are modulated by the membrane voltage in human platelets.

journal_name

Arch Biochem Biophys

journal_title

Archives of biochemistry and biophysics

authors

Albarrán L,Dionisio N,López E,Salido GM,Rosado JA

doi

10.1016/j.abb.2013.08.007

subject

Has Abstract

pub_date

2013-10-15 00:00:00

pages

130-7

issue

2

eissn

0003-9861

issn

1096-0384

pii

S0003-9861(13)00250-6

journal_volume

538

pub_type

杂志文章

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