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Angptl 4 deficiency improves lipid metabolism, suppresses foam cell formation and protects against atherosclerosis

Hironori Adachi1, Yukio Fujiwara, Tatsuya Kondo

  • 1Department of Metabolic Medicine, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan.

Biochemical and Biophysical Research Communications
|December 20, 2008
PubMed

Insights

Genetic knockout of Angiopoietin-like protein family 4 (Angptl 4) significantly reduced lipid levels and atherosclerosis in ApoE(-/-) mice. Angptl 4 deficiency also suppressed macrophage foam cell formation in vitro.

Area of Science:

  • Biochemistry
  • Cardiovascular Biology
  • Metabolic Research

Background:

  • Angiopoietin-like protein family 4 (Angptl 4) regulates lipoprotein metabolism by inhibiting lipoprotein lipase (LPL).
  • Atherosclerosis is a complex disease involving lipid metabolism and inflammatory processes in macrophages.

Purpose of the Study:

  • To investigate the role of Angptl 4 deficiency in lipid metabolism and atherosclerosis development.
  • To assess the impact of Angptl 4 knockout on atherosclerotic lesion size and macrophage foam cell formation.

Main Methods:

  • Generation of ApoE(-/-)Angptl 4(-/-) mice and comparison with ApoE(-/-)Angptl 4(+/+) controls.
  • Measurement of fasting and postprandial triglyceride (TG) levels.
  • Quantification of atherosclerotic lesion size.
  • In vitro assessment of foam cell formation in peritoneal macrophages exposed to acetylated LDL (acLDL).

Main Results:

  • ApoE(-/-)Angptl 4(-/-) mice exhibited significantly decreased fasting and postprandial TG levels compared to controls.
  • A substantial reduction (75+/-12%) in atherosclerotic lesion size was observed in ApoE(-/-)Angptl 4(-/-) mice.
  • Macrophages from Angptl 4(-/-) mice showed significantly reduced cholesteryl ester (CE) accumulation upon acLDL stimulation.

Conclusions:

  • Genetic deletion of Angptl 4 confers protection against atherosclerosis development and progression in ApoE(-/-) mice.
  • Angptl 4 deficiency suppresses macrophage foam cell formation in vitro, suggesting a role in atherogenesis.

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