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      Apolipoprotein E Regulates Primary Cultured Human Mesangial Cell Proliferation

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          Background: The role of apolipoprotein (apo) E in kidney disease is still unclear. Animal studies have been performed, but it is doubtful if the conclusions are applicable to human beings. The objective of this study was to determine how apo E acts on human kidneys using primary cultured normal human mesangial cells (NHMCs) rather than animals used in previous studies. Methods: apo E and its isoforms E2, E3 and E4, or combinations with apo B were cocultured with primary NHMCs in serum-free medium. Premix WST-1 Cell Proliferation Assay System and DNA-Prep Reagent System were used to measure the proliferation and apoptosis of NHMCs, respectively. Results: (1) apo E itself increased NHMC proliferation at 24 h of culture, while it inhibited this proliferation after 48 h. (2) At 72 h of culture, apo E alone inhibited NHMC proliferation at concentrations higher than 0.78 µg/ml in concentration-dependent manner. (3) When co-cultured with both apo E and apo B, NHMC proliferation was higher than that with apo E alone and lower than that with apo B alone. (4) At 72 h of culture, apo E2, E3 and E4 inhibited NHMC proliferation at different intensities, with no proliferative effect observed. (5) Neither apo E nor apo B caused NHMC apoptosis. Conclusion: apo E regulates primary NHMC proliferation by (1) inhibiting NHMC proliferation or reducing NHMC proliferation induced by apo B, which implies that apo E has a protective effect on the kidney, and (2) increasing the proliferation under certain conditions.

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          Most cited references 14

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          Apolipoprotein B and apolipoprotein A-I: risk indicators of coronary heart disease and targets for lipid-modifying therapy

           G Walldius,  I Jungner (2004)
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            Apolipoprotein E modulates immune activation by acting on the antigen-presenting cell.

            Apolipoprotein E (ApoE) is synthesized by a variety of cells including macrophages. These cells activate T lymphocytes by antigen presentation, while the T-cell cytokine, interferon-gamma, inhibits macrophage ApoE expression. ApoE inhibits T-cell proliferation in culture but its role in immune responses has been unclear. The ApoE-deficient (E0) mouse permits an evaluation of the immunological role of ApoE. We have analysed T-cell responses to an exogenous antigen (ovalbumin) and polyclonal mitogen (concanavalin A) in E0 and ApoE+/+ mice. Macrophages of E0 mice stimulated T-cell activation more effectively as antigen-presenting cells than macrophages from ApoE+/+ mice. Both proliferation and interferon-gamma secretion were enhanced in T cells activated in the context of antigen-presenting cells from E0 mice. Since the macrophage-T-cell interaction depends on interactions between cell surface molecules, we assessed the expression of such molecules after in vivo stimulation with interferon-gamma. This treatment caused an increased expression of the co-stimulatory surface proteins CD40 and CD80, and also of the major histocompatibility complex class II molecules I-Ab on macrophages of E0 mice compared with ApoE+/+. Our data suggest that ApoE inhibits T-cell activation by reducing the density of immune stimulatory proteins on antigen-presenting cells.
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              Apolipoprotein E and renal disease.

              Apolipoprotein E (ApoE) is a major constituent of plasma lipoproteins with many biological actions of great significance. Beyond the known influence of ApoE polymorphisms on serum lipid profile, the pathogenesis of atherosclerosis, and the development of neurodegenerative disorders, ApoE also has a major role in the pathogenesis and progression of a variety of renal diseases, as well as in the atherosclerotic complications associated with them. Briefly, the polymorphisms of ApoE are major determinants of plasma lipid levels in uremic patients. They may affect the risk for cardiovascular disease in this population, predispose to the development of diabetic nephropathy, influence the severity of certain glomerulopathies, and regulate mesangial and glomerular functions locally in the kidney microenvironment. Finally, certain mutations of the ApoE gene are associated with a recently described nephropathy, termed lipoprotein glomerulopathy.

                Author and article information

                Nephron Exp Nephrol
                Cardiorenal Medicine
                S. Karger AG
                January 2006
                23 September 2005
                : 102
                : 2
                : e62-e70
                aSecond Division of Internal Medicine, bDepartment of Molecular Oncology, Medical Faculty, Kagoshima University, and cIkeda Hospital, Kanoya, Kagoshima, Japan
                88402 Nephron Exp Nephrol 2006;102:e62–e70
                © 2006 S. Karger AG, Basel

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                Figures: 8, Tables: 1, References: 23, Pages: 1
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