Effect of oleic acid on store-operated calcium entry in immune-competent cells

• Published in: European journal of nutrition Vol. 56; no. 3; pp. 1077 - 1084
• Main Authors: Carrillo, Celia, Giraldo, María, Cavia, M. Mar, Alonso-Torre, Sara R.
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.04.2017; Springer Nature B.V
• Subjects: Calcium - metabolism; Cell Line; Chemistry; Chemistry and Materials Science; Dose-Response Relationship, Drug; Econazole - pharmacology; Fura-2 - metabolism; Humans; Jurkat Cells; Manganese - metabolism; Nutrition; Oleic Acid - pharmacology; Original Contribution; Thapsigargin - pharmacology; SOCE; signals; Oleic acid; Ca; Immune-competent cells; Ca2+ signals
• ISSN: 1436-6207; 1436-6215
• DOI: 10.1007/s00394-016-1157-5

Purpose To study the mechanism by which oleic acid (OA) (C18:1) exerts its beneficial effects on immune-competent cells. Since store-operated Ca 2+ entry (SOCE) is a Ca 2+ influx pathway involved in the control of multiple physiological processes including cell proliferation, we studied the effect of OA in Ca 2+ signals of Jurkat T cells and THP-1 monocytes, paying particular attention to SOCE. Methods Changes in [Ca 2+ ] i were measured using the Fura-2 fluorescence dye. Mn 2+ uptake was monitored as a rate of quenching of Fura-2 fluorescence measured at the Ca 2+ -insensitive wavelengths. Thapsigargin was used to induce SOCE in Fura-2-loaded cells. Results We showed a clear dose-dependent SOCE-inhibitory effect of OA in both cell lines. Such an inhibitory effect was PKC independent and totally restored by albumin, suggesting that OA exerts its effect somewhere in the membrane. We also demonstrated that OA induces increases in [Ca 2+ ] i partly mediated by an extracellular Ca 2+ influx through econazole-insensitive channels. Finally, we compared the effect of OA with stearic acid (C18:0), assuming the emerged evidence concerning the link between saturated fats and inflammation disorders. Stearic acid failed to inhibit SOCE, independently on the concentration tested, thus intensifying the physiological relevance of our findings. Conclusion We suggest a physiological pathway for the beneficial effects of OA in inflammation.