Reactive oxygen species induce proliferation of bovine aortic endothelial cells

Citation
Ja. Ruiz-gines et al., Reactive oxygen species induce proliferation of bovine aortic endothelial cells, J CARDIO PH, 35(1), 2000, pp. 109-113
Citations number
21
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
ISSN journal
01602446 → ACNP
Volume
35
Issue
1
Year of publication
2000
Pages
109 - 113
Database
ISI
SICI code
0160-2446(200001)35:1<109:ROSIPO>2.0.ZU;2-G
Abstract
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.