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High density lipoprotein suppresses lipoprotein associated phospholipase A2 in human monocytes-derived macrophages

Guan-ping Han1, Jing-yi Ren, Li Qin

  • 1Department of Cardiology, Peking University People's Hospital, Beijing, China.

Chinese Medical Journal
|December 21, 2012
PubMed
Abstract

Insights

High-density lipoprotein (HDL) effectively reduces lipoprotein-associated phospholipase A2 (Lp-PLA2) in macrophages. This study reveals HDL

Area of Science:

  • Cardiovascular Biology
  • Lipid Metabolism
  • Atherosclerosis Research

Background:

  • Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a marker of atherosclerotic plaque and promotes atherosclerosis.
  • High-density lipoprotein (HDL) is known for its anti-atherogenic properties, but its effect on Lp-PLA2 is unclear.

Purpose of the Study:

  • To investigate the effect of HDL on Lp-PLA2 expression and activity in human macrophages.
  • To elucidate the molecular mechanisms underlying HDL's regulation of Lp-PLA2.

Main Methods:

  • Human monocyte-derived macrophages were treated with varying concentrations and durations of HDL.
  • Lp-PLA2 mRNA, protein levels, and activity were assessed using RT-PCR, Western blotting, and enzyme assays.
  • The role of peroxisome proliferator-activated receptor-γ (PPARγ) was examined using pioglitazone, a PPARγ ligand.

Main Results:

  • HDL significantly inhibited Lp-PLA2 mRNA, protein expression, and activity in a dose- and time-dependent manner.
  • Pioglitazone upregulated Lp-PLA2, an effect reversed by HDL co-treatment.
  • HDL inhibited pioglitazone-induced PPARγ phosphorylation.

Conclusions:

  • HDL suppresses Lp-PLA2 expression and activity in macrophages.
  • The PPARγ pathway is implicated in HDL's inhibitory effects on Lp-PLA2.

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