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Biological Research

Print version ISSN 0716-9760

Abstract

FONCEA, ROCIO; CARVAJAL, CRISTIAN; ALMARZA, CAROLINA  and  LEIGHTON, FEDERICO. Endothelial cell oxidative stress and signal transduction. Biol. Res. [online]. 2000, vol.33, n.2, pp.86-96. ISSN 0716-9760.  http://dx.doi.org/10.4067/S0716-97602000000200008.

Endothelial dysfunction (ED) is an early event in atherosclerotic disease, preceding clinical manifestations and complications. Increased reactive oxygen species (ROS) have been implicated as important mechanisms that contribute to ED, and ROS’s may function as intracellular messengers that modulate signaling pathways. Several intracellular signal events stimulated by ROS have been defined, including the identification of two members of the mitogen activated protein kinase family (ERK1/2 and big MAP kinase, BMK1), tyrosine kinases (Src and Syk) and different isoenzymes of PKC as redox-sensitive kinases. ROS regulation of signal transduction components include the modification in the activity of transcriptional factors such as NFkB and others that result in changes in gene expression and modifications in cellular responses. In order to understand the intracellular mechanisms induced by ROS in endothelial cells (EC), we are studying the response of human umbilical cord vein endothelial cells to increased ROS generation by different pro-atherogenic stimuli. Our results show that Homocysteine (Hcy) and oxidized LDL (oxLDL) enhance the activity and expression of oxidative stress markers, such as NFkB and heme oxygenase 1. These results suggest that these pro-atherogenic stimuli increase oxidative stress in EC, and thus explain the loss of endothelial function associated with the atherogenic process

Keywords : oxidative stress; signal transduction; gene expression; endothelial cell; atherosclerosis; antioxidants.

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