MicroRNA-674-5p/5-LO axis involved in autoimmune reaction of Concanavalin A-induced acute mouse liver injury

Toxicol Lett. 2016 Sep 6:258:101-107. doi: 10.1016/j.toxlet.2016.06.010. Epub 2016 Jun 14.

Abstract

Autoimmune hepatitis is characterized, in part, by the pathways involving cysteinyl-leukotriene metabolites of arachidonic acid, the dynamics of which remain unclear. Here, we explored post-transcriptional regulation in the 5-lipoxygenase (5-LO) pathway of arachidonic acid in a Concanavalin A (Con A) induced mouse model. We found that Con A administration lead to 5-LO overexpression and cysteinyl-leukotriene release in early hepatic injury, which was attenuated by cyclosporin A pretreatment. Subsequent microarray and qRT-PCR analysis further showed that microRNA-674-5p (miR-674-5p) displayed a significant decrease in expression in Con A-damaged liver. Noting that miR-674-5p harbors a potential binding region for 5-LO, we further transfected hepatic cell lines with overexpressing miR-674-5p mimic and discovered a negative regulating effect of miR-674-5p on 5-LO expression in the presence of IL-6 or TNF-α. These findings suggest that miR-674-5p might be a negative regulator in 5-LO mediated autoimmune liver injury, representing a compelling avenue towards future therapeutic interventions.

Keywords: 5-lipoxygenase; Concanavalin A; Hepatotoxicity; miR-674-5p.

MeSH terms

  • Animals
  • Arachidonate 5-Lipoxygenase / chemistry
  • Arachidonate 5-Lipoxygenase / genetics
  • Arachidonate 5-Lipoxygenase / metabolism*
  • Cell Line
  • Concanavalin A
  • Disease Models, Animal*
  • Enzyme Induction / drug effects
  • Gene Expression Profiling
  • Gene Expression Regulation / drug effects
  • Hepatitis, Autoimmune / drug therapy
  • Hepatitis, Autoimmune / immunology
  • Hepatitis, Autoimmune / metabolism*
  • Hepatitis, Autoimmune / pathology
  • Humans
  • Immunosuppressive Agents / pharmacology
  • Interleukin-6 / metabolism
  • Leukotrienes / metabolism
  • Liver / drug effects
  • Liver / immunology
  • Liver / metabolism*
  • Liver / pathology
  • Male
  • Mice
  • Mice, Inbred BALB C
  • MicroRNAs / antagonists & inhibitors
  • MicroRNAs / metabolism*
  • Specific Pathogen-Free Organisms
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Immunosuppressive Agents
  • Interleukin-6
  • Leukotrienes
  • MIRN674 microRNA, mouse
  • MicroRNAs
  • Tumor Necrosis Factor-alpha
  • Concanavalin A
  • Arachidonate 5-Lipoxygenase