Ethanol inhibits thrombin-induced secretion by human platelets at a site distinct from phospholipase C or protein kinase C

Bénistant, Christine; Rubin, Raphael

doi:10.1042/bj2690489

Cited by 44 publications

(24 citation statements)

References 41 publications

(63 reference statements)

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“…All tend to demonstrate that alcohol added in vitro leads to a significant decrease of platelet aggregation induced by thrombin, collagen, epinephrine and ADP (17)(18)(19)(20).…”

Section: Aggregationmentioning

confidence: 99%

Alcohol, Wine and Platelet Function

Ruf¹

2004

Biol. Res.

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Epidemiological studies have demonstrated an inverse correlation between moderate wine and alcohol consumption and morbidity and mortality from coronary heart disease. The protective effect has been associated with an increase in the plasma level of HDL cholesterol, as it is well recognized that plasma HDL is inversely correlated with CHD. In addition, it has become evident that blood platelets contribute to the rate of development of atherosclerosis and CHD through several mechanisms. In recent studies it has been shown that the level of HDL cholesterol can explain only 50 % of the protective effect of alcoholic beverages; the other 50 % may be partly related to a decrease in platelet activity. This anti-platelet activity of wine is explained by ethanol but also by the polyphenolic components with which red wines are richly endowed. Several studies carried out on humans and animals have shown that wine phenolics could exert their effects by reducing prostanoid synthesis from arachidonate. In addition, it has been suggested that wine phenolics could reduce platelet activity mediated by nitric oxide. Moreover, wine phenolics increase vitamin E levels while decreasing the oxidation of platelets submitted to oxidative stress. However, a rebound phenomenon of hyperaggregability is observed after an acute alcohol consumption which is not observed with wine consumption. This protection afforded by wine has been duplicated in animals with grape phenolics added to alcohol. The rebound phenomenon may explain ischemic strokes or sudden deaths known to occur after episodes of drunkenness. It appears that wine, and wine phenolics in particular, could have a more significant inhibitory effect on platelet aggregation and could explain, in part, the hypothesis that red wine is more protective against atherosclerosis and coronary heart disease.

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“…All tend to demonstrate that alcohol added in vitro leads to a significant decrease of platelet aggregation induced by thrombin, collagen, epinephrine and ADP (17)(18)(19)(20).…”

Section: Aggregationmentioning

confidence: 99%

Alcohol, Wine and Platelet Function

Ruf¹

2004

Biol. Res.

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“…Furthermore, granule secretion and shape change can be dissociated under several experimental conditions. [21][22][23] Morphologic aspects of activation-dependent membrane fusion have been studied in detail. Platelet granules appear to undergo homotypic fusion on activation, 24 a phenomenon observed in other cells of hematopoietic origin.…”

mentioning

confidence: 99%

Subcellular distribution of 3 functional platelet SNARE proteins: human cellubrevin, SNAP-23, and syntaxin 2

Feng

Crane

Rozenvayn

et al. 2002

Blood

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Morphologic studies have demonstrated a process by which ␣-granule contents are released from platelets. Studies aimed at defining the molecular mechanisms of this release have demonstrated that SNARE proteins are required for ␣-granule secretion. These observations raise the possibility that morphologic features of ␣-granule secretion may be influenced by the subcellular distribution of SNARE proteins in the platelet. To evaluate this possibility, we analyzed the subcellular distribution of 3 functional platelet SNARE proteins-human cellubrevin, SNAP-23, and syntaxin 2. Exposure of streptolysin O-permeabilized platelets to antihuman cellubrevin antibody inhibited Ca ؉؉ -induced ␣-granule secretion by approximately 50%. Inhibition of ␣-granule secretion by antihuman cellubrevin was reversed by a blocking peptide. Syntaxin 2 and SNAP-23 have previously been demonstrated to mediate platelet granule secretion. The subcellular localization of the 3 SNARE proteins was determined by ultrastructural studies, using a pre-embedding immunonanogold method, and by immunoblot analysis of subcellular fractions. Immunonanogold localization demonstrated that approximately 80% of human cellubrevin in resting platelets was localized to platelet granule membranes. In contrast, SNAP-23 localized predominantly to plasma membrane, whereas syntaxin 2 was more evenly distributed among membranes of ␣-granules, the open canalicular system, and plasma membrane. Thus, each of these SNARE proteins has a distinct subcellular distribution in platelets, and each of these membrane compartments demonstrates a unique SNARE protein composition. IntroductionPlatelets demonstrate a number of characteristics that render them an important model of membrane trafficking. They are anucleate, display rare strands of endoplasmic reticulum, do not have Golgi structures, and synthesize little new protein. They are thought to undergo just one round of granule secretion following activation because they do not have adequate synthetic capacity to generate new granules. Although receptor-mediated 1,2 and pinocytotic 3 endocytosis have been observed in platelets, constitutive coupled endocytosis-exocytosis cycles that occur in nucleated cells in general [4][5][6][7][8] and in hematopoietic cells in particular 9 have not been documented in platelets. Thus, the degree to which generalizations regarding the molecular mechanisms of membrane trafficking can be applied to the platelet is uncertain. A second distinctive characteristic of the platelet is that its limiting membrane is characterized by a system of tunneling invaginations of the plasma membrane, termed the open canalicular system (OCS). 10,11 Evidence that the OCS is open to the extracellular environment is derived from reports using various cell-impermeant tracers. 12 The fate of the OCS on platelet activation is the subject of debate. There is evidence that the OCS undergoes evagination during platelet activation that provides an extra membrane for the formation of pseudopodia. 13,14 Others have shown th...

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“…Thus, secretion in mast cells, mammary epithelial cells, platelets, neutrophils and HL60 cells is inhibited by the addition of primary alcohols (Fig. 23, Stutchfield & Cockcroft 1993;Gruchalla et al 1990;Lin et al 1991;Benistant & Rubin 1990;Yuli et al 1982;Fensome et al 1996;Brown et al 1998;Siddhanta et al 2000;Way et al 2000;Boisgard & Chanat 2000). However, this could be due to changes other than inhibition of PA formation by PLD.…”

Section: Role In Exocytosis and Endocytosismentioning

confidence: 94%