Pexophagy is induced by increasing peroxisomal reactive oxygen species in 1′10-phenanthroline-treated cells

Doo Sin Jo, Dong Jun Bae, So Jung Park, Hae Mi Seo, Han Byeol Kim, Jeong Su Oh, Jong Wook Chang, Sang Yeob Kim, Jung Won Shin, Dong Hyung Cho

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

Although autophagy regulates the quality and quantity of cellular organelles, the regulatory mechanisms of peroxisomal autophagy remain largely unknown. In this study, we developed a cell-based image screening assay, and identified 1,10-phenanthroline (Phen) as a novel pexophagy inducer from chemical library screening. Treatment with Phen induces selective loss of peroxisomes but not endoplasmic reticulum and Golgi apparatus in hepatocytes. In addition, Phen increases autophagic engulfment of peroxisomes in an ATG5 dependent manner. Interestingly, treatment of Phen excessively produces peroxisomal reactive oxygen species (ROS), and inhibition of the ROS suppresses loss of peroxisome in Phen-treated cells. Taken together, these results suggest that Phen triggers pexophagy by enhancing peroxisomal ROS.

Original languageEnglish
Pages (from-to)354-360
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume467
Issue number2
DOIs
StatePublished - 13 Nov 2015

Keywords

  • autophagy
  • Peroxisome
  • pexophagy
  • Phenanthroline
  • ROS

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