| Literature DB >> 19094966 |
Hironori Adachi1, Yukio Fujiwara, Tatsuya Kondo, Takeshi Nishikawa, Rei Ogawa, Takeshi Matsumura, Norio Ishii, Ryoji Nagai, Keishi Miyata, Mitsuhisa Tabata, Hiroyuki Motoshima, Noboru Furukawa, Kaku Tsuruzoe, Junji Kawashima, Motohiro Takeya, Shizuya Yamashita, Gou Young Koh, Andras Nagy, Toshio Suda, Yuichi Oike, Eiichi Araki.
Abstract
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.Entities:
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Year: 2008 PMID： 19094966 DOI： 10.1016/j.bbrc.2008.12.018
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN： 0006-291X Impact factor: 3.575