miR-381 Regulates Neural Stem Cell Proliferation and Differentiation via Regulating Hes1 Expression

PLoS One. 2015 Oct 2;10(10):e0138973. doi: 10.1371/journal.pone.0138973. eCollection 2015.

Abstract

Neural stem cells are self-renewing, multipotent and undifferentiated precursors that retain the capacity for differentiation into both glial (astrocytes and oligodendrocytes) and neuronal lineages. Neural stem cells offer cell-based therapies for neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease and spinal cord injuries. However, their cellular behavior is poorly understood. MicroRNAs (miRNAs) are a class of small noncoding RNAs involved in cell development, proliferation and differentiation through regulating gene expression at post-transcriptional level. The role of miR-381 in the development of neural stem cells remains unknown. In this study, we showed that overexpression of miR-381 promoted neural stem cells proliferation. It induced the neural stem cells differentiation to neurons and inhibited their differentiation to astrocytes. Furthermore, we identified HES1 as a direct target of miR-381 in neural stem cells. Moreover, re-expression of HES1 impaired miR-381-induced promotion of neural stem cells proliferation and induce neural stem cells differentiation to neurons. In conclusion, miR-381 played important role in neural stem cells proliferation and differentiation.

Publication types

  • Retracted Publication

MeSH terms

  • Animals
  • Astrocytes / cytology
  • Basic Helix-Loop-Helix Transcription Factors / genetics*
  • Cell Differentiation / genetics*
  • Cell Proliferation / genetics*
  • Gene Expression Regulation / genetics*
  • Homeodomain Proteins / genetics*
  • MicroRNAs / physiology*
  • Neural Stem Cells / cytology*
  • Rats
  • Rats, Wistar
  • Transcription Factor HES-1

Substances

  • Basic Helix-Loop-Helix Transcription Factors
  • Hes1 protein, rat
  • Homeodomain Proteins
  • MIRN381 microRNA, rat
  • MicroRNAs
  • Transcription Factor HES-1

Grants and funding

The authors have no support or funding to report.