Lipids

, Volume 47, Issue 7, pp 647–657

Trans Fatty Acids: Induction of a Pro-inflammatory Phenotype in Endothelial Cells

  • Kevin A. Harvey
  • Candace L. Walker
  • Zhidong Xu
  • Phillip Whitley
  • Rafat A. Siddiqui
Original Article

DOI: 10.1007/s11745-012-3681-2

Cite this article as:
Harvey, K.A., Walker, C.L., Xu, Z. et al. Lipids (2012) 47: 647. doi:10.1007/s11745-012-3681-2

Abstract

Epidemiological data have shown an association of the intake of industrial produced trans fatty acids (TFA) and sudden cardiac death. The present study examines the impact of elaidic acid (t18:1n-9) and linoelaidic acid (t18:2n-6) on the human aortic endothelial cell functional response. Trans fatty acids predominately incorporated into the phospholipid component while only a minute fraction of the total fatty acids (FA) incorporated into triacylglycerol. Trans fatty acids incorporated into the plasma membranes at the expense of the saturated-FA, stearic, palmitic, and to a lesser extent, myristic acid. Both t18:1n-9 and t18:2n-6 induced a pro-inflammatory response by elevating surface expression of intercellular adhesion molecule-1 (ICAM-1). Neither oleic nor linoleic evoked a pro-inflammatory phenotype under the maximal 50 µM treatments. Both TFA and stearic acid increased phosphorylation of the ICAM-1 transcriptional regulator, nuclear factor-κβ (NF-κβ), while oleic and linoleic acids did not appear to alter the phosphorylation status. Elaidic acid minimally affected endothelial cell growth, whereas linoelaidic acid completely inhibited growth at 100 µM and imparted limited cytotoxicity up to 300 µM. Stearic acid induced cytotoxicity at concentrations above 75 µM, while oleic and linoleic acids evoked gradual dose-dependent growth inhibition with cytotoxicity occurring only at linoleic acid concentrations greater than 200 µM. In conclusion, t18:1n-9 and t18:2n-6 fatty acids effectively incorporated into the phospholipid component of endothelial cells and subsequently induce a pro-inflammatory phenotype.

Keywords

Trans fatty acidsEndothelial cellsInflammationNFκBLipid droplets

Abbreviations

ANOVA

Analysis of variance

BCA

Bicinchoninic acid

BSA

Bovine serum albumin

CHD

Coronary heart disease

CO2

Carbon dioxide

EBM2

Endothelial basal medium

EC

Endothelial cell(s)

FA

Fatty acid(s)

FBS

Fetal bovine serum

GAPDH

Glyceraldehyde 3-phosphate dehydrogenase

HAEC

Human aortic endothelial cell(s)

HUVEC

Human umbilical vein endothelial cell

ICAM-1

Intercellular adhesion molecule-1

IP-TFA

Industrially produced-trans fatty acid(s)

NF-κβ

Nuclear factor-κβ

PE

Phycoerythrin

PL

Phospholipid(s)

RP-TFA

Ruminant produced-trans fatty acid(s)

SFA

Saturated fatty acid(s)

t18:1n-9

Trans ∆9-octadeca-monoenoic acid (elaidic acid)

t18:2n-6

Trans ∆9,12-octadeca-dienoic acid (linoelaidic acid)

TAG

Triacylglycerol(s)

TBST

Tris buffered saline-tween 20

TFA

Trans fatty acid(s)

VCAM-1

Vascular cell adhesion molecule-1

Copyright information

© AOCS 2012

Authors and Affiliations

  • Kevin A. Harvey
    • 1
  • Candace L. Walker
    • 1
  • Zhidong Xu
    • 1
  • Phillip Whitley
    • 1
  • Rafat A. Siddiqui
    • 1
    • 2
    • 3
  1. 1.Cellular Biochemistry LaboratoryMethodist Research InstituteIndianapolisUSA
  2. 2.Department of MedicineIndiana University School of MedicineIndianapolisUSA
  3. 3.Indiana University Health–Methodist Hospital, Methodist Research InstituteIndianapolisUSA