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TRAP-induced platelet reactivity is inhibited by omega-3 fatty acid-derived prostaglandin E3 (PGE3)

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dc.contributor.authorOsete Albaladejo, José Miguel
dc.contributor.authorGarcía Candel, Faustino
dc.contributor.authorFernández Gómez, Francisco José
dc.contributor.authorBlanquer Blanquer, Miguel
dc.contributor.authorMarín Atucha, Noemí
dc.contributor.authorGarcía-Estañ López, Joaquín
dc.contributor.authorIyú Espinosa, David
dc.contributor.departmentFisiología
dc.contributor.otherFacultades de la UMU::Facultad de Medicina
dc.date.accessioned2026-01-20T08:58:22Z
dc.date.available2026-01-20T08:58:22Z
dc.date.copyright© 2024 by the authors
dc.date.issued2024-12-16
dc.description.abstractBackground: 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.
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dc.identifier.citationOsete, J.-M., García-Candel, F., Fernández-Gómez, F.-J., Blanquer, M., Atucha, N. M., García-Estañ, J., & Iyú, D. (2024). TRAP-Induced Platelet Reactivity Is Inhibited by Omega-3 Fatty Acid-Derived Prostaglandin E3 (PGE3). Biomedicines, 12(12), 2855. https://doi.org/10.3390/biomedicines12122855
dc.identifier.doihttps://doi.org/10.3390/biomedicines12122855
dc.identifier.eissn2227-9059
dc.identifier.urihttp://hdl.handle.net/10201/188969
dc.languageeng
dc.publisherMDPI
dc.relationSin financiación externa a la Universidad
dc.relation.publisherversionhttps://www.mdpi.com/2227-9059/12/12/2855
dc.rightsAttribution 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectProstaglandinas
dc.subjectPlaquetas
dc.subjectPprostaglandin E3
dc.subjectThrombin
dc.subjectEP3 and EP4 receptors
dc.subjectPlatelet function
dc.subjectP-selectin
dc.subjectVASP phosphorylation
dc.subject.odsObjetivo 3: Salud
dc.titleTRAP-induced platelet reactivity is inhibited by omega-3 fatty acid-derived prostaglandin E3 (PGE3)
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
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