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J. Lipid Res.
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A more recent version of this article appeared on September 1, 2004 Originally published In Press as doi:10.1194/jlr.M400069-JLR200 on June 8, 2004

Papers In Press, published online ahead of print June 1, 2004
J. Lipid Res., doi:10.1194/jlr.M400069-JLR200
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Submitted on February 18, 2004
Revised on May 11, 2004
Accepted on May 28, 2004

Endothelial lipase is synthesized by hepatic and aorta endothelial cells and its expression is altered in apoE-deficient mice

Kenneth C-W Yu, Christopher David, Sujata J. Kadambi, Andreas Stahl, Ken-Ichi Hirata, Tatsuro Ishida, Thomas Quertermous, Allen D. Cooper, and Sungshin Y. Choi

Cardiovascular Biology, Palo Alto Med. Foundation, Research Institute, Palo Alto,, CA 94301

Corresponding Author: chois{at}pamfri.org

Both LPL and HL are synthesized in parenchymal cells, secreted and bind to endothelial cells. To learn where endothelial lipase (EL) is synthesized in the adult animals the localization of EL in mouse and rat liver was studied by immunohistochemical analysis. Further, to test if EL could play a role in atherogenesis, expression of EL in the aorta and liver of apoE knockout mice was determined. EL, in both mouse and rat liver was colocalized with the vascular endothelial cells and not hepatocytes. In contrast, hepatic lipase (HL) was present in both hepatocytes and endothelial cells. By in situ hybridization EL mRNA was present only in endothelial cells in liver sections. EL was also present at low levels in the aorta of normal mice. We fed apoE knockout mice (EKO) and wild-type (WT) mice a variety of diets and determined EL expression in livers and aorta. EKO showed significant expression of EL in aorta. EL expression was lower in the liver of EKO than normal mice. Cholesterol feeding lowered EL in liver of both types of mice. In the aorta EL was higher in EKO than WT mice and cholesterol feeding had no effect. Together these data suggest that EL may be up regulated at the site of the atherosclerotic lesions and thus could supply lipids to the area.


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