Human platelets and megakaryocytes express defensin alpha 1

Xareni Valle-Jiménez, Adriana Ramírez-Cosmes, Alba Soledad Aquino-Domínguez, Francisco Sánchez-Peña, José Bustos-Arriaga, María De Los Ángeles Romero-Tlalolini, Honorio Torres-Aguilar, Jeanet Serafín-López, Sergio Roberto Aguilar Ruíz

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

16 Citas (Scopus)

Resumen

Platelets are anucleate cells that have a role in several innate immune functions, including the secretion of proteins with antimicrobial activity. Several studies have demonstrated the ability of platelets to secrete thrombin-induced platelet microbicidal proteins and antimicrobial peptides, like hBD-1. However, the expression and secretion of defensins of the alpha family by platelets have not been fully elucidated. The aim of this study was to characterize the expression of defensin alpha 1 (DEFA1) in human platelets and megakaryocytes. Our data indicate that DEFA1 mRNA and protein are present in peripheral blood platelets and in the megakaryoblastic leukemia cell line (MEG-01). DEFA1 co-localize with α-granules of platelets and MEG-01 cells, and was also detected in cytoplasm of MEG-01 cells. The assay of our in vitro model of platelet-like particles (PLPs) revealed that MEG-01 cells could transfer DEFA1 mRNA to their differentiated PLPs. Furthermore, platelets secreted DEFA1 into the culture medium when activated with thrombin, adenosine diphosphate, and lipopolysaccharide; meanwhile, MEG-01 cells secreted DEFA1 when activated with thrombopoietin. Platelet’s secreted DEFA1 can rebind to platelet’s surface and have antibacterial activity against the gram-negative bacteria Escherichia coli. In summary, our data indicate that both, human platelets and megakaryocytes, can express and secrete DEFA1. These results suggest a new role of platelets and megakaryocytes in the innate immune response.

Idioma originalInglés
Páginas (desde-hasta)344-354
Número de páginas11
PublicaciónPlatelets
Volumen31
N.º3
DOI
EstadoPublicada - 2 abr. 2020

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