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Artículo

Mediators and molecular pathways involved in the regulation of neutrophil extracellular trap formation mediated by activated platelets

Carestia, AgostinaIcon ; Kaufman, TomásIcon ; Rivadeneyra, LeonardoIcon ; Landoni, Verónica InésIcon ; Pozner, Roberto GabrielIcon ; Negrotto, SoledadIcon ; D'Atri, Lina PaolaIcon ; Gomez, Ricardo MartinIcon ; Schattner, Mirta AnaIcon
Fecha de publicación: 01/2016
Editorial: Federation of American Societies for Experimental Biology
Revista: Journal of Leukocyte Biology
ISSN: 0741-5400
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Inmunología

Resumen

In addition to being key elements in hemostasis and thrombosis, platelets amplify neutrophil function. We aimed to gain further insight into the stimuli,mediators, molecular pathways, and regulation of neutrophil extracellular trap formation mediated by human platelets. Platelets stimulated by lipopolysaccharide, a wall component of gram-negative bacteria, Pam3-cysteineserine- lysine 4, a mimetic of lipopeptide from gram-positive bacteria, Escherichia coli, Staphylococcus aureus, or physiologic platelet agonists promoting neutrophil extracellular trap formation and myeloperoxidase-associated DNA activity under static and flow conditions. Although P-selectin or glycoprotein IIb/IIIa were not involved, platelet glycoprotein Ib, neutrophil cluster of differentiation 18, and the release of von Willebrand factor and platelet factor 4 seemed to be critical for the formation of neutrophil extracellular traps. The secretion of these molecules depended on thromboxane A2 production triggered by lipopolysaccharide or Pam3-cysteine-serine-lysine 4 but not on high concentrations of thrombin. Accordingly, aspirin selectively inhibited platelet-mediated neutrophil extracellular trap generation. Signaling through extracellular signal-regulated kinase, phosphatidylinositol 3-kinase, and Src kinases, but not p38 or reduced nicotinamide adenine dinucleotide phosphate oxidase, was involved in platelet-triggered neutrophil extracellular trap release. Platelet-mediated neutrophil extracellular trap formation was inhibited by prostacyclin. Our results support a role for stimulated platelets in promoting neutrophil extracellular trap formation, reveal that an endothelium-derived molecule contributes to limiting neutrophil extracellular trap formation, and highlight platelet inhibition as a potential target for controlling neutrophil extracellular trap cell death.
Palabras clave: Platelet Factor 4 , Thromboxane A2 , Tlr Agonists , Von Willebrand Factor
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/39829
URL: https://jlb.onlinelibrary.wiley.com/doi/abs/10.1189/jlb.3A0415-161R
DOI: http://dx.doi.org/10.1189/jlb.3A0415-161R
Colecciones
Articulos(IBBM)
Articulos de INST.DE BIOTECNOLOGIA Y BIOLOGIA MOLECULAR
Articulos(IMEX)
Articulos de INST.DE MEDICINA EXPERIMENTAL
Citación
Carestia, Agostina; Kaufman, Tomás; Rivadeneyra, Leonardo; Landoni, Verónica Inés; Pozner, Roberto Gabriel; et al.; Mediators and molecular pathways involved in the regulation of neutrophil extracellular trap formation mediated by activated platelets; Federation of American Societies for Experimental Biology; Journal of Leukocyte Biology; 99; 1; 1-2016; 153-162
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