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| mice with a targeted inactivation of Abc1 display morphologic abnormalities and perturbations in their lipoprotein metabolism ( |
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Abc1 knockout (-/-) mice revealed an approximately 70% reduction in cholesterol, markedly reduced plasma phospholipids, and an almost complete lack of high density lipoproteins ( |
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Abca1-/- mice have greatly decreased apoE levels in both the cortex (80%) and the cerebrospinal fluid (98%) ( |
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cerebrospinal fluid from Abca1-/- mice had significantly reduced cholesterol as well as small apoE-containing lipoproteins ( |
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Abca1-/- astrocytes secreted lipoprotein particles that had markedly decreased cholesterol and apoE and had smaller apoE-containing particles ( |
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in both astrocytes and microglia, ABCA1 deficiency reduces lipid efflux to exogenous apoE ( |
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the impaired ability to efflux lipids in ABCA1-/- glia results in lipid accumulation in both astrocytes and microglia and apoE secretion is compromised in ABCA1-/- astrocytes and microglia ( |
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total plasma cholesterol was significantly reduced by approximately 30% in mice that lack ABCA1 exclusively in the intestine because of a significant reduction in plasma HDL cholesterol ( |
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apoA-I, apoA-II, and apoB were significantly decreased in mice that lack ABCA1 exclusively in the intestine ( |
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mice lacking both intestinal and hepatic ABCA1 displayed a further significant decrease in plasma HDL cholesterol levels ( |
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Mice deficient in displayed leukocytosis, a transplantable myeloproliferative disorder, and a dramatic expansion of the stem and progenitor cell population containing Lin(-)Sca-1(+)Kit+ (LSK) in the bone marrow ( |
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platelets in Abca1-deficient mice are slightly larger in size and exhibit aggregation and secretion defects in response to low concentrations of thrombin and collagen |