Skip directly to search Skip directly to A to Z list Skip directly to page options Skip directly to site content

NIOSHTIC-2 Publications Search

Search Results

Are mitochondrial reactive oxygen species required for autophagy?

Authors
Jiang-J; Maeda-A; Ji-J; Baty-CJ; Watkins-SC; Greenberger-JS; Kagan-VE
Source
Biochem Biophys Res Commun 2011 Aug; 412(1):55-60
NIOSHTIC No.
20039788
Abstract
Reactive oxygen species (ROS) are said to participate in the autophagy signaling. Supporting evidence is obscured by interference of autophagy and apoptosis, whereby the latter heavily relies on ROS signaling. To dissect autophagy from apoptosis we knocked down expression of cytochrome c, the key component of mitochondria-dependent apoptosis, in HeLa cells using shRNA. In cytochrome c deficient HeLa1.2 cells, electron transport was compromised due to the lack of electron shuttle between mitochondrial respiratory complexes III and IV. A rapid and robust LC3-I/II conversion and mitochondria degradation were observed in HeLa1.2 cells treated with staurosporine (STS). Neither generation of superoxide nor accumulation of H(2)O(2) was detected in STS-treated HeLa1.2 cells. A membrane permeable antioxidant, PEG-SOD, plus catalase exerted no effect on STS-induced LC3-I/II conversion and mitochondria degradation. Further, STS caused autophagy in mitochondria DNA-deficient p HeLa1.2 cells in which both electron transport and ROS generation were completely disrupted. Counter to the widespread view, we conclude that mitochondrial ROS are not required for the induction of autophagy.
Keywords
Biological-effects; Blood-analysis; Blood-cells; Catalysis; Cell-biology; Cell-differentiation; Cell-function; Cell-morphology; Cellular-reactions; Cytology; Microbiology; Molecular-biology; Molecular-structure; Oxidation; Oxidative-processes; Reaction-rates; Author Keywords: Apoptosis; Autophagy; Reactive oxygen species; Cytochrome c deficient; HeLa cells; Staurosporine
Contact
Jianfei Jiang, Center for Free Radical and Antioxidant Health, Department of Environmental and Occupational Health, University of Pittsburgh, PA 15219
CODEN
BBRCA9
Publication Date
20110819
Document Type
Journal Article
Email Address
jjf73@pitt.edu
Funding Type
Grant
Fiscal Year
2011
NTIS Accession No.
NTIS Price
Identifying No.
Grant-Number-R01-OH-008282
Issue of Publication
1
ISSN
0006-291X
Source Name
Biochemical and Biophysical Research Communications
State
WV; PA
Performing Organization
University of Pittsburgh at Pittsburgh
TOP