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Originally published In Press as doi:10.1194/jlr.M500366-JLR200 on September 30, 2005
Papers In Press, published online ahead of print December 1, 2005
J. Lipid Res., doi:10.1194/jlr.M500366-JLR200
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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