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George P. Livanos Laboratory, Critical Care Department and Pulmonary Services, Evangelismos Hospital, University of Athens, Athens 10675, Greece
Vascular endothelial growth factor (VEGF) is a potent
angiogenic stimulus, the expression of which increases in skeletal
muscle after exercise. Because exercise is also accompanied by
increased intramuscular reactive oxygen species (ROS) generation, we
tested the hypothesis that ROS stimulate VEGF production from skeletal myotubes. Differentiated C2C12 skeletal
myotubes exposed to ROS-producing agents exhibited a
concentration-dependent increase in VEGF production, whereas
undifferentiated myoblasts did not respond to oxidants. Moreover,
conditioned medium from ROS-treated myotubes increased the bovine lung
microvascular cell proliferation rate. To study the mechanism(s)
involved in the stimulation of VEGF production by ROS, myotubes were
pretreated with a selective phosphatidylinositol 3-kinase (PI3K)
inhibitor, LY-294002, before being exposed to hydrogen peroxide or
pyrogallol. LY-294002 attenuated both Akt phosphorylation and VEGF
production. In addition, oxidants increased nuclear
factor-
B-dependent promoter activity in transiently transfected myotubes; however, pretreatment with the pharmacological inhibitor of
nuclear factor-B, diethyldithiocarbamate, did not affect the oxidant-stimulated VEGF release. We conclude that ROS induce VEGF release from myotubes via a PI3K/Akt-dependent pathway.
exercise; vascular endothelial growth factor; phosphatidylinositol 3-kinase; protein kinase B
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