Mitochondrial fragmentation caused by phenanthroline promotes mitophagy

FEBS Lett. 2012 Dec 14;586(24):4303-10. doi: 10.1016/j.febslet.2012.10.035. Epub 2012 Oct 31.

Abstract

Mitochondrial dynamics and mitophagy are thought to be important events for the quality control of mitochondria and mitochondria-associated diseases. To identify novel mitophagy modulators, we developed a cell-based screening system and selected 1,10-phenanthroline (Phen) as a target molecule. Phen treatment highly induced mitochondrial fragmentation and mitochondrial dysfunctions in a Drp1 dependent manner. Phen treatment also increased autophagy. Moreover, prolonged exposure of Phen increased mitochondria clearance through mitophagy. Phen-mediated loss of mitochondrial mass was more reduced in ATG5 deficient cells than in wild type cells. In addition, down-regulation of Drp1 decreased autophagy activation, suggesting that mitochondrial fission is involved in Phen-mediated mitophagy. Thus, our results demonstrate that the disruption of mitochondrial dynamics and mitochondrial dysfunctions provokes mitophagy in Phen-treated cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autophagy-Related Protein 5
  • Cell Line
  • Chelating Agents / adverse effects*
  • Down-Regulation / drug effects
  • Dynamins / metabolism
  • GTP Phosphohydrolases / metabolism
  • Humans
  • Mice
  • Microtubule-Associated Proteins / metabolism
  • Mitochondria / drug effects*
  • Mitochondrial Dynamics / drug effects
  • Mitochondrial Proteins / metabolism
  • Mitophagy / drug effects*
  • Phenanthrolines / pharmacology*

Substances

  • ATG5 protein, human
  • Atg5 protein, mouse
  • Autophagy-Related Protein 5
  • Chelating Agents
  • Microtubule-Associated Proteins
  • Mitochondrial Proteins
  • Phenanthrolines
  • GTP Phosphohydrolases
  • DNM1L protein, human
  • Dnm1l protein, mouse
  • Dynamins
  • 1,10-phenanthroline