Abstract
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.
Original language | English (US) |
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Pages (from-to) | 2586-2594 |
Number of pages | 9 |
Journal | Journal of lipid research |
Volume | 46 |
Issue number | 12 |
DOIs | |
State | Published - Dec 2005 |
Keywords
- Apolipoprotein E
- Atherogenesis
- High density lipoprotein
- Immunohistochemistry
- In vivo
- Inflammation
- Liver
- Low density lipoprotein receptor
- Macrophage
- Reverse cholesterol transport
ASJC Scopus subject areas
- Endocrinology