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Valgimigli, M., Merli, E., Malagutti, P., Soukhomovskaia, O., Cicchitelli, G., Macri, G. and Ferrari, R. (2003) Endothelial dysfunction in acute and chronic coronary syndromes: Evidence for a pathogenetic role of oxidative stress. Archives of Biochemistry and Biophysics, 420, 255-261.
http://dx.doi.org/10.1016/j.abb.2003.07.006

has been cited by the following article:

• TITLE: Roles of NADPH oxidase 2 and 4 in endothelial cell survival and death under serum depletion

  AUTHORS: Hyeona Jeon, Yong Chool Boo

  KEYWORDS: Endothelial Cells; Apoptosis; Serum Depletion; Reactive Oxygen Species; NADPH Oxidases

  JOURNAL NAME: Advances in Biological Chemistry, Vol.4 No.1, February 10, 2014

  ABSTRACT: Oxidative stress and redox-signal pathways are known to be involved in endothelial apoptosis induced by serum depletion. However, the associated mechanism is not well understood and thus, was investigated in the present study focusing on NADPH oxidases (NOX). Serum removal from the culture medium led to an increase in reactive oxygen species (ROS) production and apoptotic death of human umbilical vein endothelial cells. Serum depletion also increased the gene expression of the NOX2 and NOX4 subunits. The selective suppression of NOX4 expression by small interfering RNA (siRNA) attenuated ROS production and cell death due to serum-depletion whereas siRNA for NOX2 increased cell death. Expression of exogenous NOX2 or NOX4 subunit alone had no significant effects on ROS production or cell death. Coexpression of the subunits of the NOX4 complex (NOX4 and p22phox) or the NOX2 complex (NOX2, p22phox, p47phox and p67phox) increased ROS production and cell death under serum-depleted conditions. This study suggests that endothelial cell survival and death are differentially regulated by expression levels of the subunits of NOX2 and NOX4 complexes.