Electron spin resonance studies of fatty acid-induced alterations in membrane fluidity in cultured endothelial cells

Angelina Alvarado Cader, D. Allan Butterfield, Bruce A. Watkins, Byung Hong Chung, Bernhard Hennig

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


Endothelial cell dysfunction has been implicated in the development of atherosclerosis. Of vital importance to the maintenance of endothelial cell integrity is the preservation of membrane functional and structural properties, such as membrane fluidity. The aim of this study was to develop a model for studying the relationship between endothelial cell integrity and membrane fluidity alterations in a well-defined cell culture setting. Alterations in membrane fluidity were assessed using electron spin resonance after labeling endothelial cells with the lipid-specific spin labels, CAT-16 and 12-nitroxide stearic acid. Endothelial cells were exposed to various 18-carbon fatty acids, i.e. stearic (18:0), oleic (18:1), linoleic (18:2), or linolenic (18:3), in addition to lipolyzed HDL (L-HDL) and benzyl alcohol. Membrane phospholipid fatty acid composition of endothelial cells supplemented with these fatty acids was analyzed using gas chromatography. All fatty acids, except 18:0, decreased membrane fluidity. A relationship between membrane fluidity and fatty acid compositional alterations in cellular phospholipids was observed. In particular, the arachidonic acid content decreased following exposure to 18:1, 18:2, or 18:3. Exposure of endothelial cells to L-HDL, lipoprotein particles which contain high levels of 18:1 and 18:2, also decreased membrane fluidity. The stabilization of cytoskeletal actin filaments by phalloidin partially prevented 18:2-induced increases in albumin transfer, thus implicating a cytoskeletal involvement in the 18:2-induced membrane fluidity changes involved in endothelial cell dysfunction. The present study shows that the exposure of endothelial cells to various lipids causes membrane fluidity alterations which may contribute to endothelial cell dysfunction and atherosclerosis.

Original languageEnglish
Pages (from-to)665-673
Number of pages9
JournalInternational Journal of Biochemistry and Cell Biology
Issue number7
StatePublished - Jul 1995

Bibliographical note

Funding Information:
Acknowledgements-Supported in part by grants from the National Institutes of Health (HL36552 and AG 108361, National Science Foundation (EHR9108764), Dairy Management, Inc., and the Kentucky Agricultural Experiment Station. The authors would like to thank Mary Kay O’Neill for statistical consultation and Mary A. Stuart and Alan Chait for review of the manuscript.


  • Electron spin resonance
  • Endothelial cells
  • Fatty acids
  • Membrane fluidity
  • Spin-labeling

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology


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