文章基本信息

标题：Endogenous apoE expression modulates HDL3 binding to macrophages
本地全文：下载
作者：Chen-Yi Lin ; Madhuri Lucas ; Theodore Mazzone 等
期刊名称：JLR Papers In Press
印刷版ISSN：0022-2275
电子版ISSN：1539-7262
出版年度：1998
卷号：39
期号：2
页码：293-301
语种：English
出版社：American Society for Biochemistry and Molecular Biology
摘要：We have previously shown that expression of a human apoE cDNA in J774 macrophages enhances cholesterol efflux to HDL₃. We have also shown that endogenous apoE expression produces a cell surface pool of apoE associated with proteoglycans. In this series of experiments, we first demonstrate the presence of a cell surface proteoglycan-associated apoE pool in human monocyte-derived macrophages. We then examine the hypothesis that endogenous expression of apoE modulates HDL₃ binding to macrophages, thereby, accounting for enhanced cholesterol efflux to HDL₃, specifically examining a role for the cell surface pool. Enhanced binding of apoE-free human HDL₃ to apoE-expressing macrophages, compared to non-expressing macrophages, was observed at 37°C and 4°C. The enhanced binding was not due to apoE secreted into the medium, as determined by experiments utilizing conditioned medium from apoE-secreting cells. Removal of the cell surface pool of apoE, however, substantially reduced the incremental HDL₃ binding produced by apoE expression. Cellular cholesterol mass measurements demonstrated that experimental conditions that reduced HDL₃ binding to apoE-expressing macrophages, did not substantially reduce cholesterol efflux to HDL₃. In summary, our results document a clear role for cell surface pool of apoE in modulating HDL₃ interaction with macrophages. The enhanced binding, however, does not appear to be a major mechanism contributing to the increased cholesterol efflux to HDL₃, which results from endogenous macrophage expression of apoE.— Lin, C-Y., M. Lucas, and T. Mazzone. Endogenous apoE expression modulates HDL₃ binding to macrophages. J. Lipid Res. 1998. 39: 293–301.
关键词：macrophages ; apolipoprotein E ; HDL₃ ; cell cholesterol homeostasis