Human cytomegalovirus (HCMV) exerts anti-apoptotic effect during early stage of infection, which provides HCMV time for propagation. We investigated pathways mediating the resistance to H2O2-induced cell death - a self-defense mechanism to remove infected cells. We found that human aortic endothelial cells (HAECs) infected with VHL/E strain of HCMV during first 3 days were resistant to H2O2 (0-2 mM) induced apoptosis. This anti-apoptotic effect may be mediated by the upregulation of Bcl-2, an anti-apoptotic protein through the activation pro-survival pathway extracellular signal regulated kinase (ERK). Through this mechanism, HCMV is able to propagate and causes endothelial dysfunction, hence vascular disease.
|Original language||English (US)|
|Number of pages||9|
|State||Published - May 15 2006|
Bibliographical noteFunding Information:
This project is supported by Grant NIH R01-HL071608 to X.L.W. Dr. Xing Li Wang is an AHA Established Investigator.
- Hydrogen peroxide