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BioMed Research International
Volume 2015, Article ID 429253, 7 pages
Research Article

Identification of pLG72-Induced Oxidative Stress Using Systemic Approaches

1Department of Clinical Laboratory, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310000, China
2Department of Biomedical Sciences Laboratory, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang, Zhejiang 322100, China
3Graduate Institute of Basic Medical Science, College of Medicine, China Medical University, Taichung 40402, Taiwan
4Department of Internal Medicine, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang, Zhejiang 322100, China
5Department of Computer Science and Information Engineering, Asia University, Taichung 41354, Taiwan

Received 1 July 2015; Revised 1 August 2015; Accepted 17 August 2015

Academic Editor: Ahmet Hacımüftüoğlu

Copyright © 2015 Maofeng Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


G72 is a schizophrenia-susceptible gene encoding a polypeptide with 153 amino acids. In 2002, it was originally proposed as an activator of D-amino acid oxidase (DAOA) that could enhance the activity of DAAO and subsequently reduce the neurotransmission of N-methyl-D-aspartate receptors. However, several controversial findings have been reported recently. Due to a number of inconsistent descriptions of pLG72’s biofunctions, this study aims to identify the cellular effects induced by pLG72 in U87 cells using systems biology approaches. The analyses of transcriptomics and biological networks showed that pLG72 might be involved in the induction of oxidative stress. To confirm the in silico prediction, we tested and discovered that overexpression of pLG72 effectively enhanced reactive oxygen species (ROS) in U87 cells and, furthermore, this induction can be quenched by Tempol, a general ROS scavenger. Therefore, G72-transgenic mice presenting some psychiatric symptoms, along with the pLG72 level being significantly increased in the serum of patients with schizophrenia, have led us to propose that the ROS enhancement in mental diseases may be from the overexpression of pLG72 in brain cells.