Inhibition of early atherogenesis in transgenic mice by human apolipoprotein AI

Article Abstract:

The health implications of cholesterol in the blood are determined by the types and quantities of cholesterol in the blood plasma. High levels of low-density lipoprotein (LDL) cholesterol are correlated with increased risk for atherosclerosis, and high levels of high-density lipoprotein (HDL) cholesterol are associated with decreased risk for atherosclerosis, and its attendant heart disease and strokes. Since the protein apolipoprotein AI (ApoA-I) is the major protein component of HDL, it is not surprising that higher amounts of ApoA-I are also associated with lower risk for disease. Since HDL cholesterol is carried back to the liver from the body tissues, it is plausible to think that higher amounts might carry back more cholesterol and provide benefit directly. However, increases in HDL cholesterol may result from some unknown factor that directly reduces the risk for atherosclerosis; if this is the case, manipulating HDL directly would have no effect on the risks for atherosclerosis. To examine the role of HDL in preventing disease, the direct physiological effects of ApoA-I have now been examined in laboratory mice. Some inbred strains of mice are predisposed to develop fatty streak lesions when fed diets rich in fats. These lesions represent the early stages of what will become atherosclerosis. Researchers examined the effect of ApoA-I on these lesions by using the techniques of molecular biology. With genetic engineering, the gene for human ApoA-I was inserted into the mouse genes. The resulting animals make all the normal mouse proteins, but they also make the human ApoA-I as well. The large amounts of ApoA-I in these mice resulted in a correspondingly large amount of HDL in the blood. It was found that the high levels of HDL actually did result in some protection, and the development of the fatty lesions in these mice was significantly inhibited. It is possible that ApoA-I may inhibit the development of mature atherosclerotic plaques as well. (Consumer Summary produced by Reliance Medical Information, Inc.)

Prevention, Physiological aspects, Apolipoproteins, High density lipoproteins, Cholesterol, Lipoproteins, Blood lipoproteins

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Atherogenesis in transgenic mice expressing human apolipoprotein(a)

Article Abstract:

The risk factors for atherosclerosis are well known, but with one exception its causes remain unclear. A study using transgenic mice that express human apolipoprotein(a) may help clarify matters. Experimental mice exposed to a high fat diet develop more lipid-staining lesions in the aorta than non-transgenic mice on a similar diet or transgenic mice on a normal diet. Apolipoprotein(a) was found to localize with lipids in lesion areas suggesting that the observed differences in atherogenesis results from the protein.

Development and progression, Genetically modified mice

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Perspectives for vascular genomics

Article Abstract:

Research is presented concerning the interactions of environmental and genetic factors which result in vascular diseases. Data from the human genome programme is applied to vascular disorders.

Usage, Human Genome Project, Cardiovascular research, Blood circulation disorders, Vascular diseases

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