title: Oleic acid inhibits stearic acid-induced inhibition of cell growth and pro-inflammatory responses in human aortic endothelial cells.
abstract: Saturated fatty acids (SFAs), significant components of both enteral/parenteral nutritional formulations (including diet), are linked to cardiovascular disease complications, such as atherosclerosis. We investigated whether oleic acid (C18:1n-9) reduces the growth inhibitory and pro-inflammatory effects of the stearic acid (C18:0) in human aortic endothelial cells (HAEC). Stearic acid induced growth inhibition at concentrations less than 50 μM, whereas higher concentrations invoked cytotoxicity. Stearic acid-induced growth inhibition and cytotoxic effects were eradicated upon cosupplementation with oleic acid (25 μM). Oleic acid (as low as 5 μM) also inhibited the stearic acid-induced increase in intercellular adhesion molecule-1 (ICAM-1) expression. Stearic acid-induced phosphorylation of nuclear factor-kappa B (NF-κB), a transcriptional regulator of ICAM-1, was also reduced by oleic acid. HAECs supplemented with either stearic or oleic acid resulted in cellular incorporation of C18:0 and C18:1n-9, respectively. Stearic acid primarily incorporated into phospholipids without increasing the total fatty acid content in HAECs. In contrast, oleic acid, with or without stearic acid, incorporated into both phospholipids and triglycerides, with a significant increase in total fatty acid amounts in triglycerides. Our data suggest that oleic acid has the ability to reduce the inflammatory effects of long-chain SFAs in HAECs through reducing cellular stearic acid incorporation and NF-κB activation.
authors.affiliation: Cellular Biochemistry Laboratory, Methodist Research Institute, Indianapolis, IN, USA.
authors.forename: Kevin A
authors.initials: KA
authors.lastname: Harvey
authors.forename: Candace L
authors.initials: CL
authors.lastname: Walker
authors.forename: Zhidong
authors.initials: Z
authors.lastname: Xu
authors.forename: Phillip
authors.initials: P
authors.lastname: Whitley
authors.forename: Thomas M
authors.initials: TM
authors.lastname: Pavlina
authors.forename: Mary
authors.initials: M
authors.lastname: Hise
authors.forename: Gary P
authors.initials: GP
authors.lastname: Zaloga
authors.forename: Rafat A
authors.initials: RA
authors.lastname: Siddiqui
mesh_terms: D001011:Aorta / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects*; D002478:Cells, Cultured; D004042:Dietary Fats, Unsaturated / Q000494:pharmacology / Q000627:therapeutic use*; D004305:Dose-Response Relationship, Drug; D042783:Endothelial Cells / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects; D016328:NF-kappa B / Q000378:metabolism; D019301:Oleic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D013229:Stearic Acids / Q000008:administration & dosage / Q000633:toxicity*; D014280:Triglycerides / Q000378:metabolism
chemical_list: D004042:Dietary Fats, Unsaturated; D016328:NF-kappa B; D013229:Stearic Acids; D014280:Triglycerides; D018799:Intercellular Adhesion Molecule-1; D019301:Oleic Acid; C031183:stearic acid