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Increased expression of inflammation-related co-stimulatory molecules by HUVECs from newborns with a strong family history of myocardial infarction stimulated with TNF-α and oxLDL

2007; Elsevier BV; Volume: 111; Issue: 2 Linguagem: Inglês

10.1016/j.imlet.2007.06.008

1879-0542

Adolfo René Méndez‐Cruz, Araceli Páez, Rafael Jiménez‐Flores, Julia Reyes‐Reali, Elvira Varela, Arturo Cérbulo‐Vázquez, Emma Rodrı́guez, Rebeca López‐Marure, Felipe A. Massó, Leopoldo Flores‐Romo, Luis F. Montaño,

Immune Response and Inflammation

Recent findings indicate that atherosclerosis, a chronic inflammatory process, might start during childhood. Nevertheless, the expression of inflammation-related molecules of endothelial cell isolated from healthy neonates with a strong family history of myocardial infarction (SFHMI) has been rarely analyzed. Human umbilical vein endothelial cells (HUVECs) from children with SFHMI were assessed for the expression of CD40 and CD40L, in the presence of TNF-α and oxLDL. The intracellular content of CD80, CXCL8 and tissue factor by HUVECs stimulated with a CD40 agonist monoclonal antibody as well as monocytes/lymphocyte adhesion to TNF-α-stimulated HUVECs was also evaluated. The basal expression of CD40 and CD40L was higher in SFHMI-positive HUVECs in comparison to controls. TNF-α and oxLDL upregulated the expression of CD40 and CD40L in SFHMI versus control HUVECs (p < 0.001). The intracellular expression of CXCL8, tissue factor and CD80 was also higher than in controls, and the adhesion of lymphocyte- and monocyte-like cells augmented upon TNF-α stimulation. It is possible that the modifications observed in the SFHMI-positive HUVECs, all of them relevant to the atherosclerosis process, may lead to early inflammatory reactions, thus contributing to the premature initiation of atherosclerotic lesions in these children.