Browsing by Subject "Plaquetas"

Now showing 1 - 5 of 5
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    Adiro ® y P-Selectina: un marcador de activación plaquetaria en prevención secundaria
    (Universidad de Murcia, Facultad de Ciencias Sociosanitarias, 2026) Gil García, Carlota; García, Juana Elvira; Romero, María de Lourdes; IES Francisco Ros Giner
    Las enfermedades cardiovasculares constituyen una de las principales causas de mortalidad en la actualidad, y la activación plaquetaria desempeña un papel clave en su desarrollo. Entre los biomarcadores de activación plaquetaria, la P-selectina destaca por su externalización tras la activación de las plaquetas. El objetivo de este trabajo es analizar si el tratamiento con ácido acetilsalicílico (Adiro®), ampliamente utilizado en prevención secundaria, modifica la expresión de P-selectina tras la estimulación plaquetaria con ADP y TRAP. Hemos estudiado una cohorte de personas de edad avanzada tratadas con Adiro® y un grupo control sano. La expresión de P-selectina se evaluó mediante citometría de flujo, tras la estimulación y el marcaje con anticuerpos específicos. Los resultados obtenidos muestran que el tratamiento con Adiro® no se asocia a una disminución significativa de la expresión de P-selectina frente a ninguno de los agonistas empleados.
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    Alteraciones de la función plaquetaria en la cirrosis hepática
    (2015) Romecín, P.; Ortiz Ruiz, María Clara; Iyú Espinosa, David; García-Estañ López, Joaquín; Marín Atucha, Noemí; Fisiología
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    Plaquetas: características ultraestructurales y su papel en la hemostasia y respuesta inflamatoria
    (Murcia: Universidad de Murcia, Servicio de Publicaciones, 1996) Bautista, María José; Carrasco, L.; Gómez-Villamandos, J. C.; Martín de las Mulas, J.; Pérez, J.; Méndez, A.; Sierra, M. A.; Facultad de Veterinaria
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    Platelet function and microvesicle generation in patients with hemophilia A
    (Wiley, 2021-01-19) Melero Amor, Antonia; Romecín, Paola; Iyú Espinosa, David; García Bernal, David; García Navaro, Esther; Moraleda Jiménez, José María; García-Estañ López, Joaquín; García Candel, Faustino; Marín Atucha, Noemí; Fisiología
    Our results do not support any effect of FVIII on platelet function in patients with severe HA treated under the regime of prophylaxis
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    TRAP-induced platelet reactivity is inhibited by omega-3 fatty acid-derived prostaglandin E3 (PGE3)
    (MDPI, 2024-12-16) Osete Albaladejo, José Miguel; García Candel, Faustino; Fernández Gómez, Francisco José; Blanquer Blanquer, Miguel; Marín Atucha, Noemí; García-Estañ López, Joaquín; Iyú Espinosa, David; Fisiología; Facultades de la UMU::Facultad de Medicina
    Background: Prostaglandins are naturally occurring local mediators that can participate in the modulation of the cardiovascular system through their interaction with Gs/Gi-coupled receptors in different tissues and cells, including platelets. Thrombin is one of the most important factors that regulates platelet reactivity and coagulation. Clinical trials have consistently shown that omega-3 fatty acid supplementation lowers the risk for cardiovascular mortality and morbidity. Since omega-3 fatty acids are the main precursors of PGE3 in vivo, it would be relevant to investigate the effects of PGE3 on Thrombin Receptor Activating Peptide (TRAP-6)-induced platelet reactivity to determine the receptors and possible mechanisms of action of these compounds. Methods: We have measured platelet aggregation, P-selectin expression, and vasodilator-stimulated phosphoprotein (VASP) phosphorylation to evaluate platelet reactivity induced by TRAP-6 to determine the effects of PGE3 on platelet function. Results: We assessed the ability of DG-041, a selective prostanoid EP3 receptor antagonist, and of ONO-AE3-208, a selective prostanoid EP4 receptor antagonist, to modify the effects of PGE3. PGE3 inhibited TRAP-6-induced platelet aggregation and activation. This inhibition was enhanced in the presence of a Gi-coupled EP3 receptor antagonist and abolished in the presence of a Gs-coupled EP4 receptor antagonist. The effects of PGE3 were directly related to changes in cAMP, assessed by VASP phosphorylation. Conclusions: The general effects of PGE3 on human platelet reactivity are the consequence of a balance between activatory and inhibitory effects at receptors that have contrary effects on adenylate cyclase. These results indicate a potential mechanism by which omega-3 fatty acids underlie cardioprotective effects.