Angiopoietin-like protein family 4 (Angptl 4) has been shown to regulate lipoprotein metabolism through the inhibition of lipoprotein lipase (LPL). We generated ApoE-/-Angptl 4-/- mice to study the effect of Angptl 4 deficiency on lipid metabolism and atherosclerosis. Fasting and postolive oil-loaded triglyceride (TG) levels were largely decreased in ApoE-/-Angptl 4-/- mice compared with and ApoE-/-Angptl 4+/+ mice. There was a significant (75 ± 12%) reduction in atherosclerotic lesion size in ApoE-/-Angptl 4-/- mice compared with ApoE-/- Angptl 4+/+ mice. Peritoneal macrophages, isolated from Angptl 4-/- mice to investigate the foam cell formation, showed a significant decrease in newly synthesized cholesteryl ester (CE) accumulation induced by acetyl low-density lipoprotein (acLDL) compared with those from Angptl 4+/+ mice. Thus, genetic knockout of Angptl 4 protects ApoE-/- mice against development and progression of atherosclerosis and strongly suppresses the ability of the macrophages to become foam cells in vitro.
|ジャーナル||Biochemical and Biophysical Research Communications|
|出版ステータス||Published - 2009 2 20|
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