Oxidative Stress Mediated-Alterations of the MicroRNA Expression Profile in Mouse Hippocampal Neurons

International Journal of Molecular Sciences

Shunjiang Xu¹  Rui Zhang¹  Jingya Niu²  Dongsheng Cui¹  Bing Xie¹  Binggui Zhang²  Kang Lu¹  Wenjun Yu¹  Xueyi Wang³ 

[1] Central Laboratory, The First Hospital of Hebei Medical University, Shijiazhuang 050031, China; E-Mails:;Department of General Surgery, Hebei Provincial Geriatric Hospital, Shijiazhuang 050031, China; E-Mails:;Institute of Mental Health, Hebei Medical University, Shijiazhuang 050031, China; E-Mail:

关键词: oxidative stress;    microRNA;    hippocampal neurons;    array analysis;    Alzheimer disease;   

DOI  :  10.3390/ijms131216945

来源: mdpi

【 摘 要 】

Oxidative stress plays a critical role in the etiology and pathogenesis of neurodegenerative disorders, and the molecular mechanisms that control the neuron response to ROS have been extensively studied. However, the oxidative stress-effect on miRNA expression in hippocampal neurons has not been investigated, and little is known on the effect of ROS-modulated miRNAs on cell function. In this study, H₂O₂ was used to stimulate the mouse primary hippocampal neurons to develop an oxidative stress cell model. The alterations of miRNAs expression were detected by microarray analysis and five miRNAs were validated by real-time RT-PCR. The bioinformatic analysis of deregulated miRNAs was performed to determine their potential roles in the pathogenesis of neurological disorders. We found that H₂O₂ mediated a total of 101 deregulated miRNAs, which mainly took part in the regulation of the MAPK pathway. Among them, miR-135b and miR-708 were up-regulated significantly and their targets were predicted to be involved in DNA recombination, protein ubiquitination, protein autophosphorylation and development of neurons. These results demonstrated that oxidative stress alters the miRNA expression profile of hippocampal neurons, and the deregulated miRNAs might play a potential role in the pathogenesis of neurodegenerative diseases, such as Alzheimer’s disease (AD).

【 授权许可】

CC BY   
© 2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.