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Free fatty acids trigger apoptosis and inhibit cell cycle progression in human vascular endothelial cells

Michaela Artwohl1, Michael Roden, Werner Waldhäusl

  • 1Department of Internal Medicine III, Division of Endocrinology and Metabolism, Waehringer Guertel 18-20, A-1090 Vienna, Austria.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|November 5, 2003
PubMed

Insights

Elevated free fatty acids (FFAs) harm endothelial cells, increasing apoptosis and cell cycle arrest. FFA structure dictates their impact on vascular dysfunction.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Cell Biology

Background:

  • Elevated plasma free fatty acid (FFA) concentrations are linked to insulin resistance and impaired endothelial function.
  • The precise mechanisms by which FFAs affect endothelial cells remain largely unelucidated.

Purpose of the Study:

  • To investigate the effects of specific FFAs on apoptosis, cell cycle distribution, and gene/protein expression in human umbilical vein endothelial cells (HUVECs).
  • To explore the relationship between FFA structure and their pro-apoptotic and cell cycle regulatory activities.

Main Methods:

  • Exposure of HUVECs to purified FFAs (100-300 micromol/l) for 24-48 hours.
  • Assessment of apoptosis, cell cycle distribution, and expression of key genes/proteins (e.g., bak, p21(WAF-1/Cip1), clusterin, IkappaBalpha, endothelin-1, endothelial NO synthase).
  • Analysis of plasma samples from individuals with varying FFA levels.

Main Results:

  • Stearic acid significantly increased endothelial apoptosis (fivefold) and induced G0/G1 cell cycle arrest.
  • Polyunsaturated FFAs (PUFAs) demonstrated proapoptotic activity at higher concentrations and contributed to cell cycle arrest.
  • All tested FFAs reduced the expression of clusterin, IkappaBalpha, endothelin-1, and endothelial NO synthase.
  • Plasma from individuals with high FFA levels markedly increased endothelial apoptosis compared to those with low FFA levels.

Conclusions:

  • FFA structure differentially influences endothelial cell apoptosis and proliferation.
  • These cellular changes induced by FFAs are implicated in the development of micro- and macrovascular dysfunction.

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