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Del Principe D.,Section of Cell Aging and Degeneration | Ruggieri A.,Istituto Superiore di Sanita | Pietraforte D.,Istituto Superiore di Sanita | Villani A.,General Pediatric and Infectious Disease Unit | And 4 more authors.
International Journal of Cardiology | Year: 2015

It has been reported that the incidence of thrombotic events can display a gender disparity. In particular, a lower thrombotic risk has been described in female gender. The mechanisms underlying this disparity are still poorly understood. Of great interest is the hypothesis that hormones, estrogen in particular, could play a key role. In fact, the possibility that some hormonal factors could protect women from thrombotic events appears well documented in literature. For instance, several studies aimed at the analysis of the impact of estrogen and estrogen receptors in thrombogenesis claim for the implication of these hormones either in megakaryocyte differentiation or, more intriguingly, directly affecting platelet integrity and function. In consideration of the absence of the nucleus, platelet susceptibility appears quite striking and probably due to the non-nuclear estrogen receptor function. In this review we briefly summarize our knowledge as concerns the role of estrogen and estrogen receptors in determining megakaryocyte/platelet functions and thrombogenicity. © 2015 Elsevier Ireland Ltd. All rights reserved. Source


Pietraforte D.,Section of Cell Aging and Gender Medicine | Vona R.,Section of Cell Aging and Gender Medicine | Marchesi A.,General Pediatric and Infectious Disease Unit | De Jacobis I.T.,General Pediatric and Infectious Disease Unit | And 3 more authors.
Antioxidants and Redox Signaling | Year: 2014

Significance: An imbalance between the production and the detoxification of reactive oxygen species and reactive nitrogen species (ROS/RNS) can be implicated in many pathological processes. Platelets are best known as primary mediators of hemostasis and can be either targets of ROS/RNS or generate radicals during cell activation. These conditions can dramatically affect platelet physiology, leading even, as an ultimate event, to the cell number modification. In this case, pathological conditions such as thrombocytosis (promoted by increased cell number) or thrombocytopenia and myelodysplasia (promoted by cell decrease mediated by accelerated apoptosis) can occur. Recent Advances: Usually, in peripheral blood, ROS/RNS production is balanced by the rate of oxidant elimination. Under this condition, platelets are in a nonadherent "resting" state. During endothelial dysfunction or under pathological conditions, ROS/RNS production increases and the platelets respond with specific biochemical and morphologic changes. Mitochondria are at the center of these processes, being able to both generate ROS/RNS, that drive redox-sensitive events, and respond to ROS/RNS-mediated changes of the cellular redox state. Irregular function of platelets and enhanced interaction with leukocytes and endothelial cells can contribute to pathogenesis of atherosclerotic and thrombotic events. Critical Issues: The relationship between oxidative stress, platelet death, and the activation-dependent pathways that drive platelet pro-coagulant activity is unclear and deserves to be explored. Future Directions: Expanding knowledge about how platelets can mediate hemostasis and modulate inflammation may lead to novel and effective therapeutic strategies for the long and growing list of pathological conditions that involve both thrombosis and inflammation. Antioxid. Redox Signal. 21, 177-193. © Copyright 2014, Mary Ann Liebert, Inc. 2014. Source


Straface E.,Istituto Superiore di Sanita | Marchesi A.,General Pediatric and Infectious Disease Unit | Gambardella L.,Istituto Superiore di Sanita | Metere A.,Istituto Superiore di Sanita | And 8 more authors.
Antioxidants and Redox Signaling | Year: 2012

The aim of the present work was to evaluate the contribution of the different reactive oxidizing species to systemic oxidative stress in the whole blood of patients with Kawasaki disease (KD). This is a rare generalized systemic vasculitis typical of the early childhood characterized by inflammation and endothelial dysfunction with a high risk for cardiovascular fatal events. We found that, compared to age-matched healthy donors, blood from KD patients showed increased production of oxygen-and nitrogen-derived species as detected by electron paramagnetic resonance (EPR) spin probing with the cyclic hydroxylamine 1-hydroxy-3-carboxy-pyrrolidine. The • NO pathway involvement was also confirmed by the decreased concentrations of the endogenous CNO synthase inhibitor asymmetric dimethyl-arginine and the increased amounts of 3-nitrotyrosine in plasma. Further, increased plasma yields of the proinflammatory enzyme myeloperoxidase were also observed. The appearance of circulating red blood cell alterations typically associated with oxidative imbalance and premature aging (e.g., decrease of total thiol content, glycophorin A, and CD47 expression, as well as increase of phosphatidylserine externalization) has also been detected. Collectively, our observations lead to hypothesize that the simultaneous oxidative and nitrative stress occurrence in the blood of KD patients may play a pathogenetic role in the cardiovascular complications often associated with this rare disease. © 2012 Mary Ann Liebert, Inc. Source

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