title: HUVECs from newborns with a strong family history of myocardial infarction overexpress adhesion molecules and react abnormally to stimulating agents.
abstract: Atherosclerosis is a complex disease involved in major fatal events such as myocardial infarction and stroke. It is the result of interactions between metabolic, dietetic and environmental risk factors acting on a genetic background that could result in endothelial susceptibility. Our aim was to determine the patterns of expression of adhesion molecules and whether phosphatidylserine is translocated to the cell surface of human umbilical vein endothelial cells (HUVECs) isolated from healthy newborns born to parents with a strong family history of myocardial infarction under TNF-alpha or oxLDL stimulated conditions. Compared to control HUVECs, experimental cords showed: (a) a four-fold increase in VCAM-1 expression under basal conditions, which showed no change after stimulation with the pro-atherogenic factors; (b) a two-fold increase in basal P-selectin expression that reached a 10-fold increase with any of the pro-atherogenic factors; (c) a basal ICAM-1 expression similar to P-selectin that was not modified by the pro-atherogenic molecules; (d) a similar PECAM-1 expression. Unexpectedly, phospathidylserine expression in experimental cord HUVECs was significantly increased (211 817 versus 3354 TFU) but was not associated to apoptotic death as the percentage of dead cells induced by TNF-alpha treatment was very low (0.55 versus 9.87% in control HUVECs). The latter result was corroborated by TUNEL staining. T cell adherence to HUVECs was highly up-regulated in the genetically predisposed samples. The analysis of nonpooled HUVECs, from newborns to family predisposed myocardial-infarction individuals, might represent a useful strategy to identify phenotypical and functional alterations, and hopefully, to take early preventive actions.
authors.affiliation: Depto. Biología Celular, Instituto Nacional de Cardiología Ignacio Chávez, Tlalpan, Mexico.
authors.forename: A
authors.initials: A
authors.lastname: Paez
authors.forename: A R
authors.initials: AR
authors.lastname: Méndez-Cruz
authors.forename: E
authors.initials: E
authors.lastname: Varela
authors.forename: E
authors.initials: E
authors.lastname: Rodriguez
authors.forename: J
authors.initials: J
authors.lastname: Guevara
authors.forename: L
authors.initials: L
authors.lastname: Flores-Romo
authors.forename: L F
authors.initials: LF
authors.lastname: Montaño
authors.forename: F A
authors.initials: FA
authors.lastname: Massó
mesh_terms: D016022:Case-Control Studies; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000097:blood*; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000737:chemistry* / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology* / Q000378:metabolism; D005312:Fetal Blood / Q000166:cytology*; D020022:Genetic Predisposition to Disease; D006801:Humans; D007231:Infant, Newborn; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D019169:Jurkat Cells; D008077:Lipoproteins, LDL / Q000494:pharmacology; D009203:Myocardial Infarction / Q000097:blood* / Q000235:genetics; D019007:P-Selectin / Q000097:blood; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000097:blood; D013268:Stimulation, Chemical; D013601:T-Lymphocytes / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D020298:U937 Cells; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood
chemical_list: D015815:Cell Adhesion Molecules; D008077:Lipoproteins, LDL; D019007:P-Selectin; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; C099252:oxidized low density lipoprotein; D018799:Intercellular Adhesion Molecule-1