Mild palmitate treatment increases mitochondrial mass but does not affect EA.hy926 endothelial cells viability

• Published in: Archives of biochemistry and biophysics 2017-11, Vol.634, p.88-95
• Main Authors: Dymkowska, Dorota, Kawalec, Maria, Wyszomirski, Tomasz, Zabłocki, Krzysztof
• Format: Article
• Language: English
• Subjects: Cell Line; Cell Survival - drug effects; Cell Survival - immunology; Dose-Response Relationship, Drug; Endothelial cells; Endothelial Cells - drug effects; Endothelial Cells - physiology; Humans; Inflammatory response; Mitochondria - drug effects; Mitochondria - physiology; Mitochondrial mass; Nitric Oxide - metabolism; Palmitate; Palmitates - administration & dosage; Reactive oxygen species; Reactive Oxygen Species - immunology
• ISSN: 0003-9861; 1096-0384
• DOI: 10.1016/j.abb.2017.10.006

A dyslipidaemia-related increase of the concentration of long-chain fatty acids in the plasma is an important pathological factor substantially increasing risk of serious consequences in vascular endothelium. Inflammatory response, atherosclerosis and insulin resistance seem the most severe. Palmitate at excessive concentrations has been shown to have a harmful effect on endothelial cells impairing NO generation, stimulating reactive oxygen species (ROS) formation and affecting their viability. On the other hand we found that palmitate applied for 48 h at 100 μM concentration which is sufficient to induce inflammatory response, increase ROS generation and reduce insulin sensitivity of EA.hy926 cells, unexpectedly also stimulates NO synthesis and increases mitochondrial mass, suggesting a pro-survival rather than anti-survival effect. This finding unveils a potential protective mechanism allowing cells to maintain their energy homeostasis under conditions of a moderate deregulation of lipid metabolism.