Roles of NADPH oxidase 2 and 4 in endothelial cell survival and death under serum depletion ()
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.
Share and Cite:
Jeon, H. and Boo, Y. (2014) Roles of NADPH oxidase 2 and 4 in endothelial cell survival and death under serum depletion.
Advances in Biological Chemistry,
4, 10-19. doi:
10.4236/abc.2014.41003.