MicroRNA-138 promotes tau phosphorylation by targeting retinoic acid receptor alpha

FEBS Lett. 2015 Mar 12;589(6):726-9. doi: 10.1016/j.febslet.2015.02.001. Epub 2015 Feb 11.

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative dementia characterized by Aβ deposition and neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau. Emerging evidence shows that microRNAs (miRNAs) contribute to the pathogenesis of AD. Herein, we investigated the role of miR-138, a brain enriched miRNA, which is increased in AD patients. We found that miR-138 is increased in AD models, including N2a/APP and HEK293/tau cell lines. Overexpression of miR-138 activates glycogen synthase kinase-3β (GSK-3β), and increases tau phosphorylation in HEK293/tau cells. Furthermore, we confirm that retinoic acid receptor alpha (RARA) is a direct target of miR-138, and supplement of RARA substantially suppresses GSK-3β activity, and reduces tau phosphorylation induced by miR-138. In conclusion, our data suggest that miR-138 promotes tau phosphorylation by targeting the RARA/GSK-3β pathway.

Keywords: Alzheimer’s disease; Glycogen synthase kinase-3β; Phosphorylation; Retinoic acid receptor alpha; Tau; miR-138.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / metabolism
  • Base Sequence
  • Binding Sites
  • Gene Expression
  • HEK293 Cells
  • Humans
  • MicroRNAs / physiology*
  • Phosphorylation
  • Protein Processing, Post-Translational
  • RNA Interference
  • Receptors, Retinoic Acid / genetics*
  • Receptors, Retinoic Acid / metabolism
  • Retinoic Acid Receptor alpha
  • tau Proteins / metabolism*

Substances

  • MAPT protein, human
  • MIRN138 microRNA, human
  • MicroRNAs
  • RARA protein, human
  • Receptors, Retinoic Acid
  • Retinoic Acid Receptor alpha
  • tau Proteins