Key result
Endothelial lipase expression causes less HDL and apoA-I reduction in apoA-I/A-II double transgenic mice.
Why the study?
Apolipoprotein A-II may inhibit the activity of enzymes involved in HDL metabolism, potentially reducing endothelial lipase's influence on HDL in vivo.
Answers are grounded in this paper and cite their sources.
ApoA-II blunts EL-mediated HDL reduction in transgenic mice; leaves open relevance to human HDL metabolism.
Endothelial lipase (EL) plays an important physiological role in modulating HDL metabolism. Data suggest that plasma contains an inhibitor of EL, and previous studies have suggested that apolipoprotein A-II (apoA-II) inhibits the activity of several enzymes involved in HDL metabolism. Therefore, we hypothesized that apoA-II may reduce the ability of EL to influence HDL metabolism. To test this hypothesis, we determined the effect of EL expression on plasma phospholipase activity and HDL metabolism in human apoA-I and human apoA-I/A-II transgenic mice. Expression of EL in vivo resulted in lower plasma phospholipase activity and significantly less reduction of HDL-cholesterol, phospholipid, and apoA-I levels in apoA-I/A-II double transgenic mice compared with apoA-I single transgenic mice. We conclude that the presence of apoA-II on HDL particles inhibits the ability of EL to influence the metabolism of HDL in vivo.
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Broedl et al. (2006) studied HDL metabolism. Endothelial lipase (EL) expression vs. apoA-I single transgenic mice was evaluated on Plasma phospholipase activity and HDL-cholesterol, phospholipid, and apoA-I levels. Expression of endothelial lipase resulted in significantly less reduction of HDL-cholesterol, phospholipid, and apoA-I levels in apoA-I/A-II double transgenic mice compared to single transgenic mice.
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