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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-alpha and oxLDL.

Authors :
Méndez-Cruz AR
Paez A
Jiménez-Flores R
Reyes-Reali J
Varela E
Cerbulo-Vazquez A
Rodriguez E
López-Marure R
Masso FA
Flores-Romo L
Montaño LF
Source :
Immunology letters [Immunol Lett] 2007 Aug 15; Vol. 111 (2), pp. 116-23. Date of Electronic Publication: 2007 Jul 23.
Publication Year :
2007

Abstract

Background: 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.<br />Methods: Human umbilical vein endothelial cells (HUVECs) from children with SFHMI were assessed for the expression of CD40 and CD40L, in the presence of TNF-alpha 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-alpha-stimulated HUVECs was also evaluated.<br />Results: The basal expression of CD40 and CD40L was higher in SFHMI-positive HUVECs in comparison to controls. TNF-alpha 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-alpha stimulation.<br />Conclusions: 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.

Details

Language :
English
ISSN :
0165-2478
Volume :
111
Issue :
2
Database :
MEDLINE
Journal :
Immunology letters
Publication Type :
Academic Journal
Accession number :
17675167
Full Text :
https://doi.org/10.1016/j.imlet.2007.06.008