Endothelial cell oxidative stress and signal transduction

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 ROSs may function as intracellular messengers that modulate...

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Autores principales:	FONCEA,ROCIO, CARVAJAL,CRISTIAN, ALMARZA,CAROLINA, LEIGHTON,FEDERICO
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2000
Materias:	oxidative stress signal transduction gene expression endothelial cell atherosclerosis antioxidants
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602000000200008
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spelling	oai:scielo:S0716-976020000002000082010-02-11Endothelial cell oxidative stress and signal transductionFONCEA,ROCIOCARVAJAL,CRISTIANALMARZA,CAROLINALEIGHTON,FEDERICO oxidative stress signal transduction gene expression endothelial cell atherosclerosis antioxidants 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 ROSs 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 processinfo:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.33 n.2 20002000-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602000000200008en10.4067/S0716-97602000000200008
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	oxidative stress signal transduction gene expression endothelial cell atherosclerosis antioxidants
spellingShingle	oxidative stress signal transduction gene expression endothelial cell atherosclerosis antioxidants FONCEA,ROCIO CARVAJAL,CRISTIAN ALMARZA,CAROLINA LEIGHTON,FEDERICO Endothelial cell oxidative stress and signal transduction
description	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 ROSs 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
author	FONCEA,ROCIO CARVAJAL,CRISTIAN ALMARZA,CAROLINA LEIGHTON,FEDERICO
author_facet	FONCEA,ROCIO CARVAJAL,CRISTIAN ALMARZA,CAROLINA LEIGHTON,FEDERICO
author_sort	FONCEA,ROCIO
title	Endothelial cell oxidative stress and signal transduction
title_short	Endothelial cell oxidative stress and signal transduction
title_full	Endothelial cell oxidative stress and signal transduction
title_fullStr	Endothelial cell oxidative stress and signal transduction
title_full_unstemmed	Endothelial cell oxidative stress and signal transduction
title_sort	endothelial cell oxidative stress and signal transduction
publisher	Sociedad de Biología de Chile
publishDate	2000
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602000000200008
work_keys_str_mv	AT foncearocio endothelialcelloxidativestressandsignaltransduction AT carvajalcristian endothelialcelloxidativestressandsignaltransduction AT almarzacarolina endothelialcelloxidativestressandsignaltransduction AT leightonfederico endothelialcelloxidativestressandsignaltransduction
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Endothelial cell oxidative stress and signal transduction

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