tailieunhanh - Báo cáo khoa học: Glycation of low-density lipoprotein results in the time-dependent accumulation of cholesteryl esters and apolipoprotein B-100 protein in primary human monocyte-derived macrophages

Nonenzymatic covalent binding (glycation) of reactive aldehydes (from glu-cose or metabolic processes) to low-density lipoproteins has been previ-ously shown to result in lipid accumulation in a murine macrophage cell line. The formation of such lipid-laden cells is a hallmark of atheroscler-osis. | ễFEBS Journal Glycation of low-density lipoprotein results in the time-dependent accumulation of cholesteryl esters and apolipoprotein B-100 protein in primary human monocyte-derived macrophages Bronwyn E. Brown1 Imran Rashid1 David M. van Reyk2 and Michael J. Davies1 3 1 Free RadicalGroup The Heart Research Institute Camperdown Sydney NSW Australia 2 Department of Health Sciences University of Technology Sydney NSW Australia 3 Faculty of Medicine University of Sydney NSW Australia Keywords aldehydes atherosclerosis foam cells human monocyte-derived macrophages low-density lipoproteins Correspondence M. J. Davies 114 Pyrmont Bridge Road Camperdown Sydney NSW 2050 Australia Fax 61 2 95655584 Tel 61 2 82088900 E-mail daviesm@ Received 12 December 2006 accepted 15 January 2007 doi Nonenzymatic covalent binding glycation of reactive aldehydes from glucose or metabolic processes to low-density lipoproteins has been previously shown to result in lipid accumulation in a murine macrophage cell line. The formation of such lipid-laden cells is a hallmark of atherosclerosis. In this study we characterize lipid accumulation in primary human monocyte-derived macrophages which are cells of immediate relevance to human atherosclerosis on exposure to low-density lipoprotein glycated using methylglyoxal or glycolaldehyde. The time course of cellular uptake of low-density lipoprotein-derived lipids and protein has been characterized together with the subsequent turnover of the modified apolipoprotein B-100 apoB protein. Cholesterol and cholesteryl ester accumulation occurs within 24 h of exposure to glycated low-density lipoprotein and increases in a time-dependent manner. Higher cellular cholesteryl ester levels were detected with glycolaldehyde-modified low-density lipoprotein than with methylglyoxal-modified low-density lipoprotein. Uptake was significantly decreased by fucoidin an inhibitor of scavenger receptor SR-A and a mAb to CD36.

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