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Unsaturated fatty acids isolated from human lipoproteins activate protein phosphatase type 2Cbeta and induce

B Hufnagel1, M Dworak, M Soufi

  • 1Department for Pharmacology and Toxicology, Philipps-University Marburg, Ketzerbach 63, D-35032 Marburg, Germany.

Atherosclerosis
|May 25, 2005
PubMed

Insights

Free fatty acids stimulate protein phosphatase type 2Cbeta (PP2Cbeta) activity, leading to endothelial cell death and apoptosis. This suggests PP2Cbeta plays a role in atherosclerosis development.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Medicine

Background:

  • Serine/threonine protein phosphatase type 2C (PP2C) activity is modulated by unsaturated fatty acids.
  • PP2C dephosphorylates Bad, influencing apoptosis.
  • Endothelial cell death is a critical factor in vascular diseases.

Purpose of the Study:

  • To investigate the role of protein phosphatase 2Cbeta (PP2Cbeta) in endothelial cell death.
  • To determine the effect of lipophilic compounds and lipoproteins on PP2Cbeta activity and endothelial cells.
  • To elucidate the mechanisms underlying PP2Cbeta-mediated endothelial apoptosis.

Main Methods:

  • Detection and colocalization of PP2Cbeta and Bad in human umbilical vein endothelial cells (HUVECs).
  • In vitro assays to assess PP2Cbeta activity in response to lipophilic compounds and lipoproteins.
  • Analysis of free fatty acids released from lipoproteins and their impact on PP2Cbeta and apoptosis.

Main Results:

  • PP2Cbeta and Bad were found to colocalize in the cytosol of HUVECs.
  • Lipophilic compounds stimulating PP2Cbeta induced HUVEC death.
  • Lipoprotein lipase-treated lipoproteins significantly increased PP2Cbeta activity and triggered HUVEC apoptosis, mediated by free fatty acids like oleic and linoleic acid.

Conclusions:

  • PP2Cbeta is present in HUVECs and participates in apoptosis.
  • Free fatty acids released from lipoproteins are key mediators of PP2Cbeta activation and endothelial cell death.
  • PP2Cbeta may be a significant factor in the pathogenesis of atherosclerosis.

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