Trans-fatty acids induce pro-inflammatory responses and endothelial cell dysfunction

Kevin A. Harvey, Tyler Arnold, Tamkeen Rasool, Caryl Antalis, Steven Miller, Rafat A. Siddiqui

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Epidemiological data indicate that there is a strong association between intake of trans -18:2 fatty acids (TFA) and sudden cardiac death. There is little known about the mechanisms by which TFA exert harmful effects on the cardiovascular system. The present in vitro study is the first to demonstrate the effects of membrane-incorporated C18:2 TFA on human aortic endothelial cell (HAEC) function. Trans-18:2 fatty acids were incorporated to a greater extent (2-fold) in the phospholipid fraction of endothelial cells than that of cis-18:2; furthermore, these fatty acids were enriched to a similar extent in the TAG fraction. Flow cytometric analysis indicated that TFA treatment of HAEC significantly increased the expression of endothelial adhesion molecules, including intercellular adhesion molecule-1 (CD54) and vitronectin receptor (CD51/CD61). Incorporation of TFA into membranes increased HAEC adhesion to fibronectin- or vitronectin-coated plates by 1.5- to 2-fold, respectively. Neutrophil and monocyte adhesion to HAEC monolayers was nearly proportional to adhesion molecule expression. TFA treatment also induced the release of monocyte chemoattractant protein-1 by nearly 3-fold in non-stimulated HAEC. Furthermore, we examined the role of TFA on in vitro angiogenic assays. Chemotactic migration of TFA-treated HAEC toward sphingosine-1-phosphate (SPP) was significantly increased compared with controls. Conversely, capillary morphogenesis of TFA-treated HAEC was significantly inhibited in response to SPP, suggesting that TFA incorporation suppresses endothelial cell differentiation. In conclusion, these in vitro studies demonstrated that TFA play a role in the induction of pro-inflammatory responses and endothelial cell dysfunction.

Original languageEnglish
Pages (from-to)723-731
Number of pages9
JournalBritish Journal of Nutrition
Volume99
Issue number4
DOIs
StatePublished - Apr 2008

Fingerprint

Trans Fatty Acids
Fatty Acids
Endothelial Cells
Integrin alphaVbeta3
Vitronectin
Membranes
Chemokine CCL2
Sudden Cardiac Death
Intercellular Adhesion Molecule-1
Cardiovascular System
Morphogenesis
Fibronectins
Cell Adhesion

Keywords

  • Adhesion molecules
  • Capillary morphogenesis
  • Chemotaxis
  • Endothelial cells
  • Trans-fatty acids

ASJC Scopus subject areas

  • Medicine (miscellaneous)

Cite this

Trans-fatty acids induce pro-inflammatory responses and endothelial cell dysfunction. / Harvey, Kevin A.; Arnold, Tyler; Rasool, Tamkeen; Antalis, Caryl; Miller, Steven; Siddiqui, Rafat A.

In: British Journal of Nutrition, Vol. 99, No. 4, 04.2008, p. 723-731.

Research output: Contribution to journalArticle

Harvey, Kevin A. ; Arnold, Tyler ; Rasool, Tamkeen ; Antalis, Caryl ; Miller, Steven ; Siddiqui, Rafat A. / Trans-fatty acids induce pro-inflammatory responses and endothelial cell dysfunction. In: British Journal of Nutrition. 2008 ; Vol. 99, No. 4. pp. 723-731.
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