Atherogenic and inflammatory profile of human arterial endothelial cells (HUAEC) in response to LDL subfractions
de Castellarnau, Conxita (Universitat de Barcelona. Departament de Biologia Cel·lular)
Bancells, Cristina (Institut d'Investigació Biomèdica Sant Pau)
Benitez, Sonia (Institut d'Investigació Biomèdica Sant Pau)
Reina, Manuel (Universitat de Barcelona. Departament de Biologia Cel·lular)
Ordóñez, J. (Jordi) 1952- (Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular)
Sanchez-Quesada, Jose Luis (Institut d'Investigació Biomèdica Sant Pau)

Data:	2007
Resum:	Background: Electronegative LDL (LDL(-)) is a minor modified LDL fraction present in plasma that has been demonstrated to be inflammatory in endothelial cells isolated from human umbilical vein (HUVEC). Methods: A protein array able to measure 42 cytokines, chemokines and related compounds involved in atherogenesis was used to determine their release into the culture medium of human arterial endothelial cells (HUAEC) activated or not by two low-density lipoprotein (LDL) fractions isolated from human plasma by anion-exchange chromatography. Results: The results of the protein array (confirmed using specific ELISAs for each induced factor) revealed that HUAEC in the absence of stimuli released small amounts of interleukin 8 (IL-8), monocyte chemotactic protein 1 (MCP-1) and growth-related oncogene (GRO). The major native LDL fraction (named LDL(+)) increased the release of these molecules and also those of interleukin 6 (IL-6) and GROα. Compared to LDL(+), the minor modified fraction, named electronegative LDL (LDL(-)), increased all these factors to a greater degree and also induced the release of granulocyte-monocyte colony-stimulating factor (GM-CSF) and platelet-derived growth factor B (PDGF-B). These results were confirmed by ELISA. Conclusions: All these results indicate that, compared to LDL(+), LDL(-) fraction promotes not only the release of proinflammatory factors but also those of atherogenic factors in endothelial cells of arterial origin, thereby suggesting a new role for LDL(-) in atherogenesis. © 2006 Elsevier B. V. All rights reserved.
Ajuts:	Ministerio de Ciencia y Tecnología SAF2001-0480 Instituto de Salud Carlos III FISC03/08 Instituto de Salud Carlos III FISC03/01 Instituto de Salud Carlos III PI030885 Instituto de Salud Carlos III CP040110 Ministerio de Ciencia y Tecnología PTQ2001-0090 Ministerio de Ciencia y Tecnología FPU2004-1468
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Llengua:	Anglès
Document:	Article ; recerca ; Versió sotmesa a revisió
Publicat a:	Clinica Chimica Acta, Vol. 376 Núm. 1-2 (january 2007) , p. 233-236, ISSN 1873-3492

DOI: 10.1016/j.cca.2006.07.024

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