Extracellular reactive oxygen species are generated by a plasma membrane oxidative phosphorylation system
- Authors
- Lee, Hyun; Kim, Bong-Woo; Lee, Jung-Woo; Hong, Jin; Lee, Jung-Wha; Kim, Hong-Lim; Lee, Jae-Seon; Ko, Young-Gyu
- Issue Date
- 11월-2017
- Publisher
- ELSEVIER SCIENCE INC
- Keywords
- Plasma membrane oxidative phosphorylation; NADH; Extracellular superoxide; Detergent-resistant lipid rafts; Insulin signaling
- Citation
- FREE RADICAL BIOLOGY AND MEDICINE, v.112, pp.504 - 514
- Indexed
- SCIE
SCOPUS
- Journal Title
- FREE RADICAL BIOLOGY AND MEDICINE
- Volume
- 112
- Start Page
- 504
- End Page
- 514
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/81635
- DOI
- 10.1016/j.freeradbiomed.2017.08.016
- ISSN
- 0891-5849
- Abstract
- Although the oxidative phosphorylation (OXPHOS) system has been found in mitochondria and the plasma membrane of various mammalian cell lines, understanding the physiological functions of the plasma membrane OXPHOS system is challenging. Here, we demonstrated that OXPHOS I, II, III, IV and V subunits were expressed in the plasma membrane of HepG2 cells and primary mouse hepatocytes, as determined by non-permeabilized immunofluorescence, total internal reflection fluorescence (TIRF) microscopy, cell surface-biotin labeling and plasma membrane and lipid raft isolation. Next, we demonstrated that NADH administration generated extracellular superoxide and improved insulin signaling in HepG2 cells and primary mouse hepatocytes. The NADH-dependent generation of extracellular superoxide was prevented by knockdown of NDUFV-1, the first subunit of OXPHOS I receiving electrons from NADH and the NADH-improved insulin signaling was abolished by extracellular catalase. Thus, we conclude that the OXPHOS system in the plasma membrane may be required for the generation of extracellular ROS and the regulation of insulin signaling.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - Graduate School > Department of Life Sciences > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.