| The focus of my research and thesis is on the inflammatory and oxidative mechanisms in endothelial activation, dysfunction and atherosclerosis. Atherogenesis shares many features with inflammatory and immunal reactions. Because of its strategic anatomic position, endothelial cells (EC) are a primary target for injury and cardiovascular risk factors. Bacterial endotoxin (LPS), together with T-lymphocytes cytokine interferon-gamma (IFN?), causes inflammation and immune response. A simple method for isolating and culturing mouse aortic endothelial cells (MAEC) is developed for studying the endothelial injury and activation by these stimuli in vitro (Section I). The effects of LPS and IFN?, in the absence and presence of hypercholesterolemia, a traditional risk factor for atherosclerosis, on endothelial function and pro-inflammatory gene expression in vivo are also studied (Section II). |