Our main research interest is the pathogenesis of plasma lipoprotein alterations and the mechanisms of early atherogensis. Early atherosclerotic lesions are characterized by recruitment of macrophages. We are focusing on the macrophage as a cell with a potential role in both lipoprotein metabolism and atherogenesis. The macrophage plays an important role in the regulation of lipoprotein metabolism and in the process of atherogenesis. It produces proteins (such as lipoprotein receptors, apoE, and lipoprotein lipase) that can control the levels of plasma cholesterol and triglycerides, and it represents a common cell type of the atherosclerotic lesion, where it eventually transforms into a foam cell, a typical finding in the early plaque. Since tissue macrophages derive from circulating monocytes, we are currently using bone marrow transplantation as a way to study the contribution of normal or genetically engineered macrophages to the regulation of lipoprotein metabolism and to the development of atherosclerosis in the mouse. We are following several areas of investigation: 1. Study the role that macrophage apoE production plays in the induction, progression, and regression of the atherosclerotic process. 2. Study the effects of over-expression of apoE by the macrophage on cholesterol levels and atherosclerosis susceptibility in mouse models of hypercholesterolemia other than apoE deficiency. 3. Dissect the role played in vivo by macrophage lipoprotein receptors (LDL receptor, scavenger receptor, and the remnant receptor) in determining progression to foam cell. 4. Analyze the use of macrophage as vehicles of proteins not normally expressed by this cell type, such as apoAI, to delay atherosclerosis. These studies have the potential to clarify the role of macrophage apoE in the control of lipoprotein metabolism and in the process of atherogenesis and will set the stage for a novel gene therapy approach to hypercholesterolemia and atherosclerosis. .
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Key: MeSH Term KeywordAcute Kidney Injury Adult Amyloid beta-Protein Precursor Anticholesteremic Agents Antigens, Ly Apolipoproteins A Aspartate Aminotransferases Berberine Brain Calcium CD36 Antigens Dietary Proteins Genotype Heterozygote Hyperuricemia Hypolipidemic Agents Hypolipoproteinemias Lac Operon Magnetic Resonance Spectroscopy Phosphatidylcholine-Sterol O-Acyltransferase Proprotein Convertase 9 Purines Receptor, TIE-1 Sequence Deletion Soy Foods Time Factors Transduction, Genetic Tumor Necrosis Factor-alpha Urban Health Vitamin E