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Down-regulation of apolipoprotein M expression is mediated by phosphatidylinositol 3-kinase in HepG2 cells

Ning Xu1, Bo Ahrén, Jingting Jiang

  • 1Section of Clinical Chemistry & Pharmacology, Department of Laboratory Medicine, Lunds University, S-221 85 Lund, Sweden. ning.xu@med.lu.se

Biochimica Et Biophysica Acta
|March 18, 2006
PubMed

Insights

Insulin and related factors inhibit apolipoprotein M (apoM) expression in liver cells. This regulation occurs through the phosphatidylinositol 3-kinase (PI3K) pathway, not MAP kinase or PPAR pathways.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Hepatology

Background:

  • Apolipoprotein M (apoM) is a protein primarily found in high-density lipoprotein (HDL) in human plasma.
  • Understanding the regulation of apoM expression is crucial for metabolic and cardiovascular research.

Purpose of the Study:

  • To investigate the regulatory mechanisms of apolipoprotein M (apoM) expression in human hepatoma cells (HepG2).
  • To determine the role of insulin, IGF-I, and related signaling pathways in controlling apoM expression.

Main Methods:

  • Utilized HepG2 cells to study apoM expression.
  • Administered insulin, IGF-I, and specific pathway inhibitors (AG1024, LY294002, PD98059).
  • Tested the effects of PPAR agonists (GW7647, GW1929, GW501516) on apoM and apoB expression.

Main Results:

  • Insulin, IGF-I, and IGF-IPP significantly inhibited apoM expression in HepG2 cells in a dose- and time-dependent manner.
  • Insulin's effect was mediated by the phosphatidylinositol 3-kinase (PI3K) pathway, as confirmed by inhibitors AG1024 and LY294002.
  • MAP kinase pathway inhibition (PD98059) did not affect insulin-induced apoM down-regulation.
  • PPAR-alpha and PPAR-gamma agonists did not influence apoM expression but inhibited apoB expression.
  • PPAR beta/delta agonist (GW501516) inhibited both apoM and apoB expression.

Conclusions:

  • Hepatic apoM expression is regulated by the PI3-kinase signaling pathway.
  • PPAR pathways are not involved in the regulation of apoM expression in HepG2 cells, although they affect apoB expression.

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