ROS in Platelet Biology: Functional Aspects and Methodological Insights

Masselli, Elena; Pozzi, Giulia; Vaccarezza, Mauro; Mirandola, Prisco; Galli, Daniela; Vitale, Marco; Carubbi, Cecilia; Gobbi, Giuliana

doi:10.3390/ijms21144866

Cited by 136 publications

(112 citation statements)

References 211 publications

(281 reference statements)

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“…H 2 O 2 also enhances aggregation induced by phospholipid-derived arachidonate [ 33 ]. Altogether, ROS are a part of the machinery used by platelets to oxidize LDL [ 37 ].…”

Section: Platelets As a Source Of Oxidized Ldlmentioning

confidence: 99%

LDL-Cholesterol and Platelets: Insights into Their Interactions in Atherosclerosis

Rogula

Szarpak²,

Filipiak‬

2021

Life

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Atherosclerosis and its complications, including acute coronary syndromes, are the major cause of death worldwide. The two most important pathophysiological mechanisms underlying atherosclerosis include increased platelet activation and increased low-density lipoproteins (LDL) concentration. In contrast to LDL, oxidized (ox)-LDL have direct pro-thrombotic properties by functional interactions with platelets, leading to platelet activation and favoring thrombus formation. In this review, we summarize the currently available evidence on the interactions between LDL-cholesterol and platelets, which are based on (i) the presence of ox-LDL-binding sites on platelets, (ii) generation of ox-LDL by platelets and (iii) the role of activated platelets and ox-LDL in atherosclerosis. In addition, we elaborate on the clinical implications of these interactions, including development of the new therapeutic possibilities. The ability to understand and modulate mechanisms governing interactions between LDL-cholesterol and platelets may offer new treatment strategies for atherosclerosis prevention.

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“…H 2 O 2 also enhances aggregation induced by phospholipid-derived arachidonate [ 33 ]. Altogether, ROS are a part of the machinery used by platelets to oxidize LDL [ 37 ].…”

Section: Platelets As a Source Of Oxidized Ldlmentioning

confidence: 99%

LDL-Cholesterol and Platelets: Insights into Their Interactions in Atherosclerosis

Rogula

Szarpak²,

Filipiak‬

2021

Life

View full text Add to dashboard Cite

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“…Platelets produce ROS primarily through NAD(P)H-oxidase (NOX) after exposure to agonists; the ROS thus produced regulate the activation of αIIbβ3 integrin but have a minimal impact on the secretion from α- and dense-granules and the shape changes of platelets [ 74 ]. Human platelets express both NOX1 and NOX2 [ 79 ], which differentially regulate platelet reactivity [ 80 , 81 ]. Platelets produce O 2 − when they are exposed to anoxia–reoxygenation conditions and aggregate [ 82 ].…”

Section: Oxidative Stress In the Pe-induced Prothrombotic Statementioning

confidence: 99%

Oxidative Stress and Preeclampsia-Associated Prothrombotic State

et al. 2020

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Preeclampsia (PE) is a common obstetric disease characterized by hypertension, proteinuria, and multi-system dysfunction. It endangers both maternal and fetal health. Although hemostasis is critical for preventing bleeding complications during pregnancy, delivery, and post-partum, PE patients often develop a severe prothrombotic state, potentially resulting in life-threatening thrombosis and thromboembolism. The cause of this thrombotic complication is multi-factorial, involving endothelial cells, platelets, adhesive ligands, coagulation, and fibrinolysis. Increasing evidence has shown that hemostatic cells and factors undergo oxidative modifications during the systemic inflammation found in PE patients. However, it is largely unknown how these oxidative modifications of hemostasis contribute to development of the PE-associated prothrombotic state. This knowledge gap has significantly hindered the development of predictive markers, preventive measures, and therapeutic agents to protect women during pregnancy. Here we summarize reports in the literature regarding the effects of oxidative stress and antioxidants on systemic hemostasis, with emphasis on the condition of PE.

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“…On the other hand, CCCP augments mitochondrial ROS generation [ 40 , 41 ]. This elevated ROS can oxidize a main component of the inner mitochondrial membrane, cardiolipin and induce apoptosis through ΔΨm depolarization, mitochondrial Bax translocation, cytochrome C release, caspase-3 activation and PS exposure [ 42 , 43 ]. However, given the fact that ROS scavenger, NAC can inhibit CCCP-induced reduction of ΔΨm and Bax translocation, presumably here ROS generation precedes the loss of mitochondrial transmembrane potential [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Collagen-dependent platelet dysfunction and its relevance to either mitochondrial ROS or cytosolic superoxide generation: a question about the quality and functional competence of long-stored platelets

et al. 2020

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Background: Upon vascular damage, the exposed subendothelial matrix recruits circulating platelets to site of injury while inducing their firm adhesion mainly via GPVI-collagen interaction. GPVI also supports aggregatory and pro-coagulant functions in arterial shear rate even on the matrix other than collagen. Reactive oxygen species (ROS) modulate these stages of thrombosis; however augmented oxidant stress also disturbs platelet functions. Storeddependent platelet lesion is associated with the increasing levels of ROS. Whether ROS accumulation is also relevant to collagen-dependent platelet dysfunction is the main interest of this study. Methods: Fresh PRP-PCs (platelet concentrates) were either stimulated with potent ROS-inducers PMA and CCCP or stored for 5 days. Intra-platelet superoxide (O 2 −−) or mitochondrial-ROS and GPVI expression were detected by flowcytometery. GPVI shedding, platelet aggregation and spreading/adhesion to collagen were analyzed by western blot, aggregometry and fluorescence-microscopy, respectively. Results: Mitochondrial-ROS levels in 5 days-stored PCs were comparable to those induced by mitochondrial uncoupler, CCCP while O 2 −− generations were higher than those achieved by PMA. Shedding levels in 5 daysstored PCs were higher than those induced by these potent stimuli. GPVI expressions were reduced comparably in CCCP treated and 5 days-stored PCs. Platelet adhesion was also diminished during storage while demonstrating significant reverse correlation with GPVI shedding. However, only firm adhesion (indicated by platelets spreading or adhesion surface area) was relevant to GPVI expression. Platelet adhesion and aggregation also showed reverse correlations with both O2 −− and mitochondrial-ROS formations; nonetheless mitochondrial-ROS was only relevant to firm adhesion.

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ROS in Platelet Biology: Functional Aspects and Methodological Insights

Cited by 136 publications

References 211 publications

LDL-Cholesterol and Platelets: Insights into Their Interactions in Atherosclerosis

LDL-Cholesterol and Platelets: Insights into Their Interactions in Atherosclerosis

Oxidative Stress and Preeclampsia-Associated Prothrombotic State

Collagen-dependent platelet dysfunction and its relevance to either mitochondrial ROS or cytosolic superoxide generation: a question about the quality and functional competence of long-stored platelets

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