| Summary: | <p>Atherosclerotic vascular disease is the leading cause of disease worldwide. It is an inflammatory condition affecting the arterial wall, and lesions are composed of vascular and immune cells. The purpose of this study is to understand how oxidised low density lipoprotein, a key risk factor for the development of atherosclerosis, affects immune and vascular cells involved in formation of the atherosclerotic lesion. Recent insights into the pathogenesis of atherosclerosis have highlighted changes in expression and activity of gene regulatory proteins (transcription factors) and epigenetic modifications, such as alterations in chromatin accessibility and histone marks, as important mechanisms of atherogenesis. To understand how these changes come about in atherosclerosis, genome-wide approaches have been used to investigate changes in gene expression, chromatin accessibility, and histone marks following exposure of primary human aortic endothelial cells, aortic vascular smooth muscle cells, CD4+ lymphocytes and CD14+ monocytes to oxidised low density lipoprotein.</p>
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