Difference between revisions of "Umbrasas 2019 MitoFit Preprint Arch EA"
(Created page with "{{MitoFit page name}} {{Publication |title=Umbrasas Danielius, Vanagas T, Cizas P, Borutaite V (2019) Itaconic acid decreases mitochondrial respiration and ROS generation in b...") Β |
|||
Line 9: | Line 9: | ||
|year=2019 | |year=2019 | ||
|journal=MitoFit Preprint Arch | |journal=MitoFit Preprint Arch | ||
|abstract= | |abstract=Itaconic acid (IA) is a recently discovered mammalian metabolite which is produced by macrophages upon pro-inflammatory activation: in quiescent bone marrow β derived macrophages (BMDMs). IA is hardly detectable but upon lipopolysaccharide (LPS) stimulation it reaches millimolar concentrations [1]. Recently reported physiological roles of IA include inhibition of bacterial enzyme isocitrate lyase (bactericidal activity) and the inhibition of a Krebs cycle enzyme succinate dehydrogenase (SDH) in the host cells (which has been shown for BMDMs) [2,3]. By inhibiting SDH, IA regulates succinate (a pro-inflammatory metabolite) levels thus remodelling the host cells metabolism during inflammation [3]. Microglia are macrophages residing in the brain, however, it is not clear whether these cells can also produce IA. In general, there has been very little research on IA effects on brain tissue. Therefore, in this study, we investigated whether IA exerts an effect on brain mitochondrial respiration and ROS generation and whether IA is neurotoxic. | ||
|keywords= | |keywords= | ||
|editor=[[Iglesias-Gonzalez J]] | |editor=[[Iglesias-Gonzalez J]] | ||
Line 23: | Line 23: | ||
== Preprints for [[Gentle Science]] == | == Preprints for [[Gentle Science]] == | ||
{{MitoFit preprint}} | {{MitoFit preprint}} | ||
Revision as of 16:46, 3 June 2019
Umbrasas 2019 MitoFit Preprint Arch EA
Umbrasas Danielius, Vanagas T, Cizas P, Borutaite V (2019) Itaconic acid decreases mitochondrial respiration and ROS generation in brain tissue. MitoFit Preprint Arch doi:10.26124/mitofit:EA19.MiPSchool.0001. |
Β»
Itaconic acid decreases mitochondrial respiration and ROS generation in brain tissue
Umbrasas Danielius, Vanagas T, Cizas P, Borutaite V (2019) MitoFit Preprint Arch
Abstract: Itaconic acid (IA) is a recently discovered mammalian metabolite which is produced by macrophages upon pro-inflammatory activation: in quiescent bone marrow β derived macrophages (BMDMs). IA is hardly detectable but upon lipopolysaccharide (LPS) stimulation it reaches millimolar concentrations [1]. Recently reported physiological roles of IA include inhibition of bacterial enzyme isocitrate lyase (bactericidal activity) and the inhibition of a Krebs cycle enzyme succinate dehydrogenase (SDH) in the host cells (which has been shown for BMDMs) [2,3]. By inhibiting SDH, IA regulates succinate (a pro-inflammatory metabolite) levels thus remodelling the host cells metabolism during inflammation [3]. Microglia are macrophages residing in the brain, however, it is not clear whether these cells can also produce IA. In general, there has been very little research on IA effects on brain tissue. Therefore, in this study, we investigated whether IA exerts an effect on brain mitochondrial respiration and ROS generation and whether IA is neurotoxic.
β’ Bioblast editor: Iglesias-Gonzalez J
References
- Meiser J, Kraemer L, Jaeger C, Madry H, Link A, Lepper PM, Hiller K, Schneider JG (2018) Itaconic acid indicates cellular but not systemic immune system activation. Oncotarget;9(63):32098-32107.
- Michelucci A, Cordes T, Ghelfi J, Pailot A, Reiling N, Goldmann O, Binz T, Wegner A, Tallam A, Rausell A, Buttini M, Linster CL, Medina E, et al. (2013) Immune-responsive gene 1 protein links metabolism to immunity by catalyzing itaconic acid production. Proc Natl Acad Sci U S A.; 110:7820β5.
- Lampropoulou V, Sergushichev A, Bambouskova M, Nair S, Vincent EE, Loginicheva E, Cervantes-Barragan L, Ma X, Huang SC, Griss T, Weinheimer CJ, Khader S, Randolph GJ, et al. (2016) Itaconate Links Inhibition of Succinate Dehydrogenase with Macrophage Metabolic Remodeling and Regulation of Inflammation. Cell Metab; 24:158β66.
- Gnaiger E., Kuznetsov A.V., Schneeberger S., Seiler R., Brandacher G., Steurer W., Margreiter R. (2000) Mitochondria in the Cold. In: Heldmaier G., Klingenspor M., editors. Life in the Cold. Springer; Heiderlberg, Germany: pp. 431β442.
Preprints for Gentle Science
Β» MitoFit Preprints - the Open Access preprint server for mitochondrial physiology and bioenergetics