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STAT3 Regulates Mouse Neural Progenitor Proliferation and Differentiation by Promoting Mitochondrial Metabolism

  • Su, Yixun1, 2, 3
  • Zhang, Wenjun4
  • Patro, C. Pawan K.2, 5
  • Zhao, Jing3
  • Mu, Tianhao2, 5
  • Ma, Zhongnan6, 7, 8
  • Xu, Jianqiang6
  • Ban, Kenneth2
  • Yi, Chenju1
  • Zhou, Yi2, 3, 7
  • 1 The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen , (China)
  • 2 Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore , (Singapore)
  • 3 Neurobiology Programme, Life Sciences Institute, National University of Singapore, Singapore , (Singapore)
  • 4 School of Medicine, Indiana University, Indianapolis, IN , (United States)
  • 5 Cancer Science Institute of Singapore, Singapore , (Singapore)
  • 6 Department of Biology, Southern University of Science and Technology, Shenzhen , (China)
  • 7 West China Hospital, Sichuan University, Chengdu , (China)
  • 8 Model Animal Research Center of Nanjing University, Nanjing , (China)
Published Article
Frontiers in Cell and Developmental Biology
Frontiers Media SA
Publication Date
May 19, 2020
DOI: 10.3389/fcell.2020.00362
  • Cell and Developmental Biology
  • Original Research


The proliferation and differentiation of neural progenitor lay the foundation for brain development. In neural progenitors, activation of Signal Transducer and Activator of Transcription 3 (STAT3) has been found to promote proliferation and astrocytogenesis while suppressing neurogenesis. However, our study found that Stat3 conditional knockout in neural progenitors (Stat3 cKO) also results in increased proliferation and suppressed neurogenesis. To investigate how STAT3 regulates these processes, we attempted to identify potential STAT3 target genes by RNA-seq profiling of the control (CTL) and Stat3 cKO neural progenitors. We found that STAT3 promotes the expression of genes involved in the mitochondrial oxidative phosphorylation (OXPHOS), and thereby promotes mitochondrial respiration and negatively regulates reactive oxygen species (ROS) production. In addition, we demonstrated that Stat3 loss-of-function promotes proliferation via regulation of mitochondrial metabolism and downstream signaling pathways. Our study provides novel insights into the relation between STAT3, mitochondrial metabolism and the process of embryonic neurogenesis.

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