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Study Results from Lung and Blood Institute Update Understanding of Lipids

2013 JAN 21 (NewsRx) -- By a News Reporter-Staff News Editor at Cardiovascular Week -- Researchers detail new data in Lipids. According to news reporting originating in Bethesda, Maryland, by NewsRx journalists, research stated, "The role of endothelial ABCA1 expression in reverse cholesterol transport (RCT) was examined in transgenic mice, using the endothelial-specific Tie2 promoter. Human ABCA1 (hABCA1) was significantly expressed in endothelial cells (EC) of most tissues except the liver."

The news reporters obtained a quote from the research from Lung and Blood Institute, "Increased expression of ABCA1 was not observed in resident peritoneal macrophages. ApoA-I-mediated cholesterol efflux from aortic EC was 2.6-fold higher (p <0.0001) for cells from transgenic versus control mice. On normal chow diet, Tie2 hABCA1 transgenic mice had a 25% (p <0.0001) increase in HDL-cholesterol (HDL-C) and more than a 2-fold increase of eNOS mRNA in the aorta (p <0.04). After 6 months on a high-fat, high-cholesterol (HFHC) diet, transgenic mice compared with controls had a 40% increase in plasma HDL-C (p <0.003) and close to 40% decrease in aortic lesions (p <0.02). Aortas from HFHC-fed transgenic mice also showed gene expression changes consistent with decreased inflammation and apoptosis. Beneficial effects of the ABCA1 transgene on HDL-C levels or on atherosclerosis were absent when the transgene was transferred onto ApoE or Abca1 knockout mice."

According to the news reporters, the research concluded: "In summary, expression of hABCA1 in EC appears to play a role in decreasing diet-induced atherosclerosis in mice and is associated with increased plasma HDL-C levels and beneficial gene expression changes in EC."

For more information on this research see: Endothelial expression of human ABCA1 in mice increases plasma HDL cholesterol and reduces diet-induced atherosclerosis. Journal of Lipid Research, 2012;53(1):158-67. Journal of Lipid Research can be contacted at: Amer Soc Biochemistry Molecular Biology Inc, 9650 Rockville Pike, Bethesda, MD 20814-3996, USA. (American Society for Biochemistry and Molecular Biology - www.asbmb.org; Journal of Lipid Research - www.jlr.org/)

Our news correspondents report that additional information may be obtained by contacting B.L. Vaisman, Cardiovascular-Pulmonary Branch, National Heart, Lung and Blood Institute, Clinical Center, National Institutes of Health, Bethesda, MD, United States.

The publisher of the Journal of Lipid Research can be contacted at: Amer Soc Biochemistry Molecular Biology Inc, 9650 Rockville Pike, Bethesda, MD 20814-3996, USA.

Keywords for this news article include: Lipids, Bethesda, Maryland, United States, Atherosclerosis, HDL Cholesterol, Arteriosclerosis, HDL Lipoproteins, Cardiovascular Diseases, North and Central America, Arterial Occlusive Diseases.

Our reports deliver fact-based news of research and discoveries from around the world. Copyright 2013, NewsRx LLC