Abstract
Both LPL and HL are synthesized in parenchymal cells, are secreted, and bind to endothelial cells. To learn where endothelial lipase (EL) is synthesized in adult animals, the localization of EL in mouse and rat liver was studied by immunohistochemical analysis. Furthermore, to test whether EL could play a role in atherogenesis, the expression of EL in the aorta and liver of apolipoprotein E knockout (EKO) mice was determined. EL in both mouse and rat liver was colocalized with vascular endothelial cells but not with hepatocytes. In contrast, 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 aorta of normal mice. We fed EKO mice and wild-type mice a variety of diets and determined EL expression in liver and aorta. EKO mice showed significant expression of EL in aorta. EL expression was lower in the liver of EKO mice than in normal mice. Cholesterol feeding decreased EL in liver of both types of mice. In the aorta, EL was higher in EKO than in wild-type mice, and cholesterol feeding had no effect. Together, these data suggest that EL may be upregulated at the site of atherosclerotic lesions and thus could supply lipids to the area.
Highlights
Both LPL and HL are synthesized in parenchymal cells, are secreted, and bind to endothelial cells
Because liver is the major organ in lipoprotein metabolism and endothelial lipase (EL) expression was detected at a high level in the liver by Northern blot analysis [1], we studied the localization of EL using rat and mouse liver sections
To learn where EL is localized in the liver, we performed a series of immunohistochemical experiments using anti-EL antibodies
Summary
Both LPL and HL are synthesized in parenchymal cells, are secreted, and bind to endothelial cells. EL in both mouse and rat liver was colocalized with vascular endothelial cells but not with hepatocytes. We fed EKO mice and wild-type mice a variety of diets and determined EL expression in liver and aorta. Cholesterol feeding decreased EL in liver of both types of mice. EL was higher in EKO than in wild-type mice, and cholesterol feeding had no effect. Together, these data suggest that EL may be upregulated at the site of atherosclerotic lesions and could supply lipids to the area.—Yu, K. Endothelial lipase is synthesized by hepatic and aorta endothelial cells and its expression is altered in apoEdeficient mice.
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