Impaired oxidative phosphorylation regulates necroptosis in human lung epithelial cells. Academic Article uri icon

Overview

MeSH

  • AMP-Activated Protein Kinases
  • Acrylamides
  • Adenosine Triphosphate
  • Apoptosis
  • Carbonyl Cyanide m-Chlorophenyl Hydrazone
  • Cell Respiration
  • Cells, Cultured
  • Humans
  • Mitochondria
  • Necrosis
  • Oligomycins
  • Oligopeptides
  • Sulfonamides

MeSH Major

  • Epithelial Cells
  • Lung
  • Oxidative Phosphorylation

abstract

  • Cellular metabolism can impact cell life or death outcomes. While metabolic dysfunction has been linked to cell death, the mechanisms by which metabolic dysfunction regulates the cell death mode called necroptosis remain unclear. Our study demonstrates that mitochondrial oxidative phosphorylation (OXPHOS) activates programmed necrotic cell death (necroptosis) in human lung epithelial cells. Inhibition of mitochondrial respiration and ATP synthesis induced the phosphorylation of mixed lineage kinase domain-like protein (MLKL) and necroptotic cell death. Furthermore, we demonstrate that the activation of AMP-activated protein kinase (AMPK), resulting from impaired mitochondrial OXPHOS, regulates necroptotic cell death. These results suggest that impaired mitochondrial OXPHOS contributes to necroptosis in human lung epithelial cells. Copyright © 2015 Elsevier Inc. All rights reserved.

publication date

  • August 28, 2015

has subject area

  • AMP-Activated Protein Kinases
  • Acrylamides
  • Adenosine Triphosphate
  • Apoptosis
  • Carbonyl Cyanide m-Chlorophenyl Hydrazone
  • Cell Respiration
  • Cells, Cultured
  • Epithelial Cells
  • Humans
  • Lung
  • Mitochondria
  • Necrosis
  • Oligomycins
  • Oligopeptides
  • Oxidative Phosphorylation
  • Sulfonamides

Research

keywords

  • Journal Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1016/j.bbrc.2015.07.054

PubMed ID

  • 26187663

Additional Document Info

start page

  • 875

end page

  • 880

volume

  • 464

number

  • 3