Influenza virus aggravates the ox-LDL-induced apoptosis of human endothelial cells via promoting p53 signaling.

Oxidized low-density lipoprotein (ox-LDL) is well recognized to play a key role in the development of atherosclerosis. And influenza virus infection has been also recognized to promote the atherosclerosis onset and progressing. However, little is known about the mechanism into it. In present study, we investigated the infection of A/Porto Rico/8/1934 (H1N1) (PR8) influenza virus in human endothelial Eahy926 cells, and determined the induction of apoptosis by the virus infection in the cell. Then we investigated the apoptosis induced by ox-LDL in Eahy926 cells, determined the influence of influenza virus infection on the ox-LDL-induced apoptosis in Eahy926 cells. Results demonstrated that PR8 virus infected human endothelial Eahy926 cells, forming plaques and replicated efficiently in the cell. And the virus infection promoted apoptosis in the cell, upregulated cytchrome c release, activated caspase 3. And what's more, we found that combined PR8 virus infection and ox-LDL treatment promoted higher level of apoptosis and higher level of the activation of apoptosis-associated molecules. Further examination indicated that the p53 signaling was more significantly promoted by both treatments. Therefore, present study confirmed that influenza virus aggravated the ox-LDL-induced apoptosis of human endothelial Eahy926 cells via promoting p53 signaling.