Deletion of Annexin A1 in Mice Upregulates the Expression of Its Receptor, Fpr2/3, and Reactivity to the AnxA1 Mimetic Peptide in Platelets

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Autor(es): dc.contributorNational University of Singapore-
Autor(es): dc.contributorUniversity of Reading-
Autor(es): dc.contributorCity University of Hong Kong-
Autor(es): dc.contributorUniversidade de São Paulo (USP)-
Autor(es): dc.contributorUniversidade Estadual Paulista (UNESP)-
Autor(es): dc.creatorZharkova, Olga-
Autor(es): dc.creatorSalamah, Maryam F.-
Autor(es): dc.creatorBabak, Maria V.-
Autor(es): dc.creatorRajan, Elanchezhian-
Autor(es): dc.creatorLim, Lina H. K.-
Autor(es): dc.creatorAndrade, Frans-
Autor(es): dc.creatorGil, Cristiane D.-
Autor(es): dc.creatorOliani, Sonia M.-
Autor(es): dc.creatorMoraes, Leonardo A.-
Autor(es): dc.creatorVaiyapuri, Sakthivel-
Data de aceite: dc.date.accessioned2025-08-21T19:17:01Z-
Data de disponibilização: dc.date.available2025-08-21T19:17:01Z-
Data de envio: dc.date.issued2023-07-29-
Data de envio: dc.date.issued2023-07-29-
Data de envio: dc.date.issued2023-01-31-
Fonte completa do material: dc.identifierhttp://dx.doi.org/10.3390/ijms24043424-
Fonte completa do material: dc.identifierhttp://hdl.handle.net/11449/248431-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/11449/248431-
Descrição: dc.descriptionAnnexin A1 (ANXA1) is an endogenous protein, which plays a central function in the modulation of inflammation. While the functions of ANXA1 and its exogenous peptidomimetics, N-Acetyl 2-26 ANXA1-derived peptide (ANXA1Ac2-26), in the modulation of immunological responses of neutrophils and monocytes have been investigated in detail, their effects on the modulation of platelet reactivity, haemostasis, thrombosis, and platelet-mediated inflammation remain largely unknown. Here, we demonstrate that the deletion of Anxa1 in mice upregulates the expression of its receptor, formyl peptide receptor 2/3 (Fpr2/3, orthologue of human FPR2/ALX). As a result, the addition of ANXA1Ac2-26 to platelets exerts an activatory role in platelets, as characterised by its ability to increase the levels of fibrinogen binding and the exposure of P-selectin on the surface. Moreover, ANXA1Ac2-26 increased the development of platelet-leukocyte aggregates in whole blood. The experiments carried out using a pharmacological inhibitor (WRW4) for FPR2/ALX, and platelets isolated from Fpr2/3-deficient mice ascertained that the actions of ANXA1Ac2-26 are largely mediated through Fpr2/3 in platelets. Together, this study demonstrates that in addition to its ability to modulate inflammatory responses via leukocytes, ANXA1 modulates platelet function, which may influence thrombosis, haemostasis, and platelet-mediated inflammation under various pathophysiological settings.-
Descrição: dc.descriptionBritish Heart Foundation-
Descrição: dc.descriptionImmunology Program Department of Physiology Yong Loo Lin School of Medicine National University of Singapore-
Descrição: dc.descriptionSchool of Pharmacy University of Reading-
Descrição: dc.descriptionDepartment of Chemistry City University of Hong Kong-
Descrição: dc.descriptionDepartment of Morphology and Genetics Federal University of São Paulo (UNIFESP)-
Descrição: dc.descriptionDepartment of Biology Instituto de Biociências Letras e Ciências Exatas (IBILCE) São Paulo State University (UNESP), São Paulo-
Descrição: dc.descriptionDepartment of Biology Instituto de Biociências Letras e Ciências Exatas (IBILCE) São Paulo State University (UNESP), São Paulo-
Descrição: dc.descriptionBritish Heart Foundation: PG/19/62/34593-
Idioma: dc.languageen-
Relação: dc.relationInternational Journal of Molecular Sciences-
???dc.source???: dc.sourceScopus-
Palavras-chave: dc.subjectannexin A1-
Palavras-chave: dc.subjectANXA1Ac2-26-
Palavras-chave: dc.subjectFPR2/ALX-
Palavras-chave: dc.subjectinflammation-
Palavras-chave: dc.subjectthromboinflammation-
Palavras-chave: dc.subjectthrombosis-
Título: dc.titleDeletion of Annexin A1 in Mice Upregulates the Expression of Its Receptor, Fpr2/3, and Reactivity to the AnxA1 Mimetic Peptide in Platelets-
Tipo de arquivo: dc.typelivro digital-
Aparece nas coleções:Repositório Institucional - Unesp

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