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Palmitic acid suppresses apolipoprotein M gene expression via the pathway of PPARβ/δ in HepG2 cells

Guanghua Luo1, Yuanping Shi1, Jun Zhang1

  • 1Comprehensive Laboratory, The Third Affiliated Hospital of Soochow University, Changzhou 213003, PR China.

Biochemical and Biophysical Research Communications
|February 11, 2014
PubMed

Insights

Palmitic acid inhibits apolipoprotein M (APOM) gene expression in liver cells. This down-regulation is mediated through the peroxisome proliferator-activated receptor beta/delta (PPARβ/δ) pathway.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Apolipoprotein M (APOM) is a vasculoprotective component of high-density lipoprotein (HDL), contributing to HDL's anti-atherosclerotic properties.
  • Understanding APOM expression regulation is crucial for elucidating its in vivo pathophysiological roles.
  • Previous research identified various regulators of APOM expression, including platelet-activating factor (PAF), transforming growth factors (TGF), insulin-like growth factor (IGF), leptin, and hyperglycemia.

Purpose of the Study:

  • To investigate the effect of palmitic acid on APOM gene expression in HepG2 cells.
  • To elucidate the molecular pathway(s) involved in palmitic acid-induced regulation of APOM expression.

Main Methods:

  • HepG2 cells were treated with palmitic acid.
  • The impact of palmitic acid on APOM gene expression was assessed.
  • Specific inhibitors for PI-3 kinase (LY294002), protein kinase C (GFX), and peroxisome proliferator-activated receptor beta/delta (PPARβ/δ) (GSK3787) were used to probe the underlying signaling pathways.

Main Results:

  • Palmitic acid significantly inhibited APOM gene expression in HepG2 cells.
  • Inhibition of PI-3 kinase (PI3K) or protein kinase C (PKC) did not alter the down-regulation of APOM expression induced by palmitic acid.
  • A PPARβ/δ antagonist (GSK3787) completely reversed the palmitic acid-induced down-regulation of APOM expression.

Conclusions:

  • Palmitic acid down-regulates APOM gene expression in HepG2 cells.
  • The mechanism of palmitic acid-induced APOM down-regulation involves the PPARβ/δ pathway.
  • These findings highlight a novel regulatory role of fatty acids in APOM expression with potential implications for cardiovascular health.
Keywords:
Apolipoprotein MPI-3 kinasePalmitic acidPeroxisome proliferator-activated receptor beta/deltaProtein kinase C

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