The effects of reactive oxygen species (ROS) on different cellular types ar
e variable. In some conditions they can be harmful metabolites, but they ca
n also act as intracellular messengers that are able to activate different
transcription factors. Based on previous reports in which ROS were shown to
stimulate the proliferation of mesenchymal cells, this study was carried o
ut to assess this effect on bovine aortic endothelial cells (BAECs). When c
ells were incubated with glucose oxidase (GO), an enzyme that generates H2O
2 continuously, a significant increase in BAEC proliferation was detected,
BAEC proliferation was measured by the incorporation of [H-3]thymidine in t
he DNA of BAECs, and also by an increase in the number of cells. The effect
observed with GO was maximal at 8-24 h. Catalase abolishes proliferation.
We also tested the ability of GO to phosphorylate tyrosine residues in endo
thelial cell proteins. A significant increase in tyrosine phosphorylation w
as found, which might constitute the molecular basis for proliferative effe
ct of GO. In conclusion, these results demonstrate the ability of H2O2 to s
timulate BAEC proliferation at least under certain experimental conditions.
We suggest a general activation of the cascade of tyrosine phosphorylation
as one of the possible cellular mechanisms responsible for GO-induced BAEC
proliferation.