Long Noncoding RNA EBF3-AS Promotes Neuron Apoptosis in Alzheimer's Disease

DNA Cell Biol. 2018 Mar;37(3):220-226. doi: 10.1089/dna.2017.4012. Epub 2018 Jan 3.

Abstract

Alzheimer's disease (AD) is the most common form of dementia; its pathophysiological mechanism remains unclear. Long noncoding RNAs (lncRNAs) play key roles in AD. lncRNA EBF3-AS has been found dysregulated in AD, which is abundantly expressed in the brain. The aim of this study was to investigate the role of EBF3-AS in AD. Results showed that the expressions of lncRNA EBF3-AS and EBF3 (early B cell factor 3) were upregulated in hippocampus of APP/PS1 mice (AD model mice). EBF3-AS knockdown by siRNA inhibited the apoptosis induced by Aβ25-35 and okadaic acid (OA) in SH-SY5Y. The expression of EBF3 was downregulated in Aβ25-35- and OA-treated SH-SY5Y, which was reversed by EBF3-AS knockdown. EBF3 knockdown can reverse the Aβ25-35-induced apoptosis in SH-SY5Y. These results revealed that lncRNA EBF3-AS promoted neuron apoptosis in AD, and involved in regulating EBF3 expression. EBF3-AS may be a new therapeutic target for treatment of AD.

Keywords: Alzheimer's disease; SH-SY5Y; lncRNA EBF3-AS; neurons apoptosis.

MeSH terms

  • Alzheimer Disease / genetics*
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / physiology
  • Animals
  • Apoptosis*
  • Cell Line, Tumor
  • Gene Expression
  • Hippocampus / metabolism
  • Hippocampus / pathology
  • Humans
  • Male
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Neurons / physiology*
  • RNA Interference
  • RNA, Long Noncoding / physiology*
  • Transcription Factors / genetics*
  • Transcription Factors / metabolism

Substances

  • Amyloid beta-Peptides
  • EBF3 protein, human
  • RNA, Long Noncoding
  • Transcription Factors