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Papers In Press, published online ahead of print December 1, 2005
J. Lipid Res., doi:10.1194/jlr.M500366-JLR200

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Journal of Lipid Research, Vol. 46, 2586-2594, December 2005
Copyright © 2005 by American Society for Biochemistry and Molecular Biology

Endothelial lipase modulates HDL but has no effect on atherosclerosis development in apoE^–/– and LDLR^–/– mice

Kerry W. S. Ko, Antoni Paul, Ke Ma, Lan Li and Lawrence Chan¹

Department of Medicine and Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030

The online version of this article (available at http://www.jlr.org) contains an additional table.

Published, JLR Papers in Press, September 30, 2005. DOI 10.1194/jlr.M500366-JLR200

¹ To whom correspondence should be addressed. e-mail: lchan{at}bcm.tmc.edu

Endothelial lipase (EL) is a determinant of high density lipoprotein-cholesterol (HDL-C) level, which is negatively correlated with atherosclerosis susceptibility. We found no difference in aortic atherosclerotic lesion areas between 26-week-old EL^+/+ apolipoprotein E-deficient (apoE^–/–) and EL^–/– apoE^–/– mice. To more firmly establish the role of EL in atherosclerosis, we extended our study to EL^–/– and EL^+/+ low density lipoprotein receptor-deficient (LDLR^–/–) mice that were fed a Western diet. Morphometric analysis again revealed no difference in atherosclerosis lesion area between the two groups. Compared with EL^+/+ mice, we found increased HDL-C in EL^–/– mice with apoE^–/– or LDLR^–/– background but no difference in macrophage content between lesions of EL^–/– and EL^+/+ mice in apoE^–/– or LDLR^–/– background. EL inactivation had no effect on hepatic mRNAs of proteins involved in reverse cholesterol transport. A survey of lipid homeostasis in EL^+/+ and EL^–/– macrophages revealed that oxidized LDL-induced ABCA1 was attenuated in EL^–/– macrophages. This potentially proatherogenic change may have nullified any minor protective increase of HDL in EL^–/– mice.

Thus, although EL modulated lipoprotein profile in mice, there was no effect of EL inactivation on atherosclerosis development in two hyperlipidemic atherosclerosis-prone mouse models.

Abbreviations: apoE, apolipoprotein E; EL, endothelial lipase; FPLC, fast-protein liquid chromatography; IDL, intermediate density lipoprotein; HDL-C, high density lipoprotein-cholesterol; LDLR, low density lipoprotein receptor; OxLDL, oxidized low density lipoprotein; SR-A, scavenger receptor A; SR-BI, scavenger receptor class B type I

Supplementary key words atherogenesis • in vivo • immunohistochemistry • liver • macrophage • reverse cholesterol transport • inflammation • high density lipoprotein • apolipoprotein E • low density lipoprotein receptor

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