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

Authors
Jo, D.S.[Jo, D.S.]Bae, D.-J.[Bae, D.-J.]Park, S.J.[Park, S.J.]Seo, H.M.[Seo, H.M.]Kim, H.B.[Kim, H.B.]Oh, J.S.[Oh, J.S.]Chang, J.W.[Chang, J.W.]Kim, S.-Y.[Kim, S.-Y.]Shin, J.-W.[Shin, J.-W.]Cho, D.-H.[Cho, D.-H.]
Issue Date
2015
Keywords
Peroxisome; autophagy; pexophagy; ROS; Phenanthroline
Citation
Biochemical and Biophysical Research Communications, v.467, no.2, pp.354 - 360
Journal Title
Biochemical and Biophysical Research Communications
Volume
467
Number
2
Start Page
354
End Page
360
URI
https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/48825
DOI
10.1016/j.bbrc.2015.09.153
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. © 2015 Elsevier Inc. All rights reserved.
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