Hecker 2018 Biochim Biophys Acta

From Bioblast
Jump to: navigation, search
Publications in the MiPMap
Hecker M, Sommer N, Foch S, Hecker A, Hackstein H, Witzenrath M, Weissmann N, Seeger W, Mayer K (2018) Resolvin E1 and its precursor 18R-HEPE restore mitochondrial function in inflammation. Biochim Biophys Acta 1863:1016-28.

» PMID: 29902569

Hecker M, Sommer N, Foch S, Hecker A, Hackstein H, Witzenrath M, Weissmann N, Seeger W, Mayer K (2018) Biochim Biophys Acta

Abstract: Inflammatory disorders such as sepsis are a major cause of morbidity and mortality. Mitochondrial dysfunction is considered a key factor in the pathogenesis of severe inflammation. In the present study, we aimed to investigate the impact of arachidonic acid, omega-3 (n-3) fatty acids, and n-3-derived lipid mediators 18R-HEPE and resolvin (Rv) E1 on mitochondrial function in experimental inflammation. The results revealed that, in contrast to n-6 and n-3 fatty acids, both 18R-HEPE and RvE1 possess anti-inflammatory and anti-apoptotic properties. Both mediators are able to restore inflammation-induced mitochondrial dysfunction, which is characterized by a decrease in mitochondrial respiration and membrane potential, as well as an imbalance of mitochondrial fission and fusion. Furthermore, inhibition of mitochondrial fission by Mdivi-1 and Dynasore reduces levels of the pro-inflammatory cytokines IL-6 and IL-8. These results suggest a novel functional mechanism for the beneficial effects of RvE1 in inflammatory reactions.

Keywords: Fission, Fusion, Inflammation, Mitochondria, Resolvin Bioblast editor: Kandolf G O2k-Network Lab: DE Giessen Weissmann N


Labels: MiParea: Respiration, mt-Structure;fission;fusion, Exercise physiology;nutrition;life style, mt-Medicine, Pharmacology;toxicology  Pathology: Sepsis 

Organism: Human  Tissue;cell: Blood cells  Preparation: Intact cells 


Coupling state: LEAK, ROUTINE, ET  Pathway: ROX  HRR: Oxygraph-2k 

Labels, 2018-08, PBMCs