MiR-17-92 Cluster Regulates Adult Hippocampal Neurogenesis, Anxiety, and Depression Academic Article uri icon


MeSH Major

  • Cerebral Cortex
  • Gene Expression Regulation
  • MicroRNAs
  • Tumor Suppressor Protein p53


  • Emerging evidence has shown that noncoding RNAs,¬†particularly microRNAs (miRNAs), contribute to the pathogenesis of mood and anxiety disorders, although the molecular mechanisms are poorly understood. Here, we show that altered levels of miR-17-92 in adult hippocampal neural progenitors have a significant impact on neurogenesis and anxiety- and depression-related behaviors in mice. miR-17-92 deletion in adult neural progenitors decreases neurogenesis in the dentate gyrus, while its overexpression increases neurogenesis. miR-17-92 affects neurogenesis by regulating genes in the glucocorticoid pathway, especially serum- and glucocorticoid-inducible protein kinase-1 (Sgk1). miR-17-92 knockout mice show anxiety- and depression-like behaviors, whereas miR-17-92 overexpressing mice exhibit anxiolytic and antidepression-like behaviors. Furthermore, we show that miR-17-92 expression in the adult mouse hippocampus responds to chronic stress, and miR-17-92 rescues proliferation defects induced by corticosterone in hippocampal neural progenitors. Our study uncovers a crucial role for miR-17-92 in adult neural progenitors through regulation of neurogenesis and anxiety- and depression-like behaviors.

publication date

  • November 3, 2015



  • Academic Article



  • eng

PubMed Central ID

  • PMC4981532

Digital Object Identifier (DOI)

  • 10.1016/j.celrep.2016.06.101

PubMed ID

  • 27477270

Additional Document Info

start page

  • 1653

end page

  • 63