Individuals with an imbalance in the amount of cholesterol associated with the carrier complexes HDL and LDL have an increased risk of developing cardiovascular disease, a class of diseases that affect the heart and or blood vessels, including atherosclerosis.
In this context, high levels of HDL protect against cardiovascular disease, but the mechanisms behind this protection are poorly understood.
New insight into the antiatherogenic effects of HDL is provided by a study in mice by Laurent Yvan-Charvet and colleagues at Columbia University New York.
HDL is known to promote the efflux of cholesterol from cells known as macrophage foam cells via two proteins known as ABCA1 and ABCG1.
Previous studies examining the role of each of these proteins individually have produced conflicting results as to the importance of this process for the antiatherogenic effects of HDL.
In this study, mice lacking both ABCA1 and ABCG1 were generated.
When bone marrow from these mice was transplanted into mice susceptible to developing atherosclerosis the recipients developed atherosclerosis more rapidly than recipients of normal bone marrow or bone marrow lacking either ABCA1 or ABCG1.
These data indicate that efflux of cholesterol via ABCA1 and ABCG1 is central to the antiatherogenic properties of HDL.
Article: Combined deficiency of ABCA1 and ABCG1 promotes foam cell accumulation and accelerates atherosclerosis in mice, Journal of Clinical Investigation, November 8, 2007
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