Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2052905 | FEBS Letters | 2006 | 9 Pages |
Abstract
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.
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Authors
Jing Wang, Ying H. Shen, Budi Utama, Jian Wang, Scott A. LeMaire, Joseph S. Coselli, Greg M. Vercellotti, Xing Li Wang,