Reactive oxygen and nitrogen species modulate the ex-vivo effects of LPS on platelet adhesion to fibrinogen

Casarin, André Luis; Lopes-Pires, Maria Elisa; Morganti, Rafael P.; Antunes, Edson; Marcondes, Sisi

doi:10.1016/j.lfs.2011.09.004

Cited by 8 publications

(7 citation statements)

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“…4). This finding agrees with the reports of lack of effect of LPS [21] and TNFa [22] in platelets isolated from mice, though others have observed spontaneous platelet activation upon LPS stimulation [23]. We note that these conflicting studies were conducted with platelets from species other than mice, suggesting that interspecies differences may be involved in the different responses.…”

Section: Effect Of Ascorbate On Plasminogen Activator Inhibitor-1 Prosupporting

confidence: 91%

Effect of ascorbate on plasminogen activator inhibitor-1 expression and release from platelets and endothelial cells in an in-vitro model of sepsis

Swarbreck

Secor

Ellis

et al. 2015

Blood Coagulation &Amp; Fibrinolysis

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Section: Effect Of Ascorbate On Plasminogen Activator Inhibitor-1 Prosupporting

confidence: 91%

Effect of ascorbate on plasminogen activator inhibitor-1 expression and release from platelets and endothelial cells in an in-vitro model of sepsis

Swarbreck

Secor

Ellis

et al. 2015

Blood Coagulation &Amp; Fibrinolysis

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“…Blood platelet activation plays a critical role in LPS-induced thrombocytopenia and tissue damage. Activated platelets produce ROS that cause damage of the vascular endothelium and promote multiple organ dysfunctions in sepsis (Casarin et al 2011, Tyml 2011. Some studies showed that LPS stimulates platelet secretion of dense and alpha granules, and release of biological active inflammatory mediators (Zhang et al 2009).…”

Section: Platelets Contribution In Inflammatory Processesmentioning

confidence: 99%

The physiology of blood platelets and changes of their biological activities in multiple sclerosis

Wachowicz¹,

Morel²,

Miller³

et al. 2016

Acta Neurobiologiae Experimentalis

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Increasing evidence indicates that blood platelets contribute to diverse processes that extend beyond hemostasis. Many of the same mechanisms that play a role in hemostasis and thrombosis facilitate platelets the participation in other physiological and pathological processes, particularly in the inflammation, the immune response and central nervous system disorders. Platelets are involved in pathophysiology of central nervous system diseases, especially in the pathogenesis of multiple sclerosis, but their role appears to be neglected. Platelets contribute to the inflammation and cooperate with immune cells in inflammatory and immune responses. These blood cells were identified in inflamed spinal cord and in the brain in chronic active lesions of multiple sclerosis and in the related animal models referred as Experimental Autoimmune Encephalomyelitis. This review summarizes recent insights in the platelet activation accompanied by the exocytosis of bioactive compounds stored in granules, formation of platelet microparticles, expression of specific membrane receptors, synthesis of numerous biomediators, generation of free radicals, and introduces the mechanisms by which activated platelets may be involved in the pathophysiology of multiple sclerosis. Understanding the role of platelets in multiple sclerosis may be essential for improved therapies.

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“…Lipopolysaccharide (LPS) from the cell envelope of Gram-negative bacteria is a principal cause of the symptoms of sepsis and this can result in platelet sequestration in the lungs and liver, thrombocytopenia and disseminated intravascular coagulation (DIC) [ 2 , 3 ]. LPS has been reported to modulate the function of platelets [ 4 , 5 , 6 ], although the underlying mechanisms of LPS action remain unclear. Indeed, some studies have indicated that exposure of platelets to LPS in vitro potentiates platelet function [ 7 , 8 ], while others have indicated that it supresses their activity [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide potentiates platelet responses via toll-like receptor 4-stimulated Akt-Erk-PLA2 signalling

et al. 2017

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Lipopolysaccharide (LPS) from the cell envelope of Gram-negative bacteria is a principal cause of the symptoms of sepsis. LPS has been reported to modulate the function of platelets although the underlying mechanisms of LPS action in these cells remain unclear. Platelets express the Toll-like receptor 4 (TLR4) which serves as a receptor for LPS, although the potential role of TLR4 and associated cell signalling in controlling platelet responses to LPS has not been extensively explored. In this study, we therefore investigated the actions of LPS prepared from different strains of Escherichia coli on platelet function, the underlying signalling mechanisms, and the potential role of TLR4 in orchestrating these. We report that LPS increased the aggregation of washed platelets stimulated by thromboxane (U46619) or GPVI collagen receptor agonists, effects that were prevented by a TLR4 antagonist. Associated with this, LPS enhanced fibrinogen binding, P-selectin exposure and reactive oxygen species (ROS) release. Increase of ROS was found to be important for the actions of LPS on platelets, since these were inhibited in the presence of superoxide dismutase or catalase. The effects of LPS were associated with phosphorylation of Akt, ERK1/2 and PLA2 in stimulated platelets, and inhibitors of PI3-kinase, Akt and ERK1/2 reduced significantly LPS enhanced platelet function and associated ROS production. Furthermore, inhibition of platelet cyclooxygenase or the thromboxane receptor, revealed an important role for thromboxane A2. We therefore conclude that LPS increases human platelet activation through a TLR4-PI3K-Akt-ERK1/2-PLA2 -dependent pathway that is dependent on ROS and TXA2 formation.

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Reactive oxygen and nitrogen species modulate the ex-vivo effects of LPS on platelet adhesion to fibrinogen

Cited by 8 publications

References 50 publications

Effect of ascorbate on plasminogen activator inhibitor-1 expression and release from platelets and endothelial cells in an in-vitro model of sepsis

Effect of ascorbate on plasminogen activator inhibitor-1 expression and release from platelets and endothelial cells in an in-vitro model of sepsis

The physiology of blood platelets and changes of their biological activities in multiple sclerosis

Lipopolysaccharide potentiates platelet responses via toll-like receptor 4-stimulated Akt-Erk-PLA2 signalling

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