TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000373970
  • Gene Name:DKK1
  • mRNA database:Ensembl
  • mRNA expression :down-regulated
  • mRNA Method:qRT-PCR
  • mRNA Pathway:NA
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:DB01238
  • Drug Name:Aripiprazole
  • Drug Method:down-regulated the gene expression

Disease basic infommation

  • Disease:psychiatric diseases
  • Tissue:cell line NTera2/cloneD1

Other information

  • Title:Transcriptional Effects of Psychoactive Drugs on Genes Involved in Neurogenesis
  • Journal:International Journal of Molecular Sciences
  • Published:2020
  • PubMed ID:33172123
  • Abstract:Although neurogenesis is affected in several psychiatric diseases, the effects and mechanisms of action of psychoactive drugs on neurogenesis remain unknown and/or controversial. This study aims to evaluate the effects of psychoactive drugs on the expression of genes involved in neurogenesis. Neuronal-like cells (NT2-N) were treated with amisulpride (10 碌M), aripiprazole (0.1 碌M), clozapine (10 碌M), lamotrigine (50 碌M), lithium (2.5 mM), quetiapine (50 碌M), risperidone (0.1 碌M), or valproate (0.5 mM) for 24 h. Genome wide mRNA expression was quantified and analysed using gene set enrichment analysis, with the neurogenesis gene set retrieved from the Gene Ontology database and the Mammalian Adult Neurogenesis Gene Ontology (MANGO) database. Transcription factors that are more likely to regulate these genes were investigated to better understand the biological processes driving neurogenesis. Targeted metabolomics were performed using gas chromatography-mass spectrometry. Six of the eight drugs decreased the expression of genes involved in neurogenesis in both databases. This suggests that acute treatment with these psychoactive drugs negatively regulates the expression of genes involved in neurogenesis in vitro. SOX2 and three of its target genes (CCND1, BMP4, and DKK1) were also decreased after treatment with quetiapine. This can, at least in part, explain the mechanisms by which these drugs decrease neurogenesis at a transcriptional level in vitro. These results were supported by the finding of increased metabolite markers of mature neurons following treatment with most of the drugs tested, suggesting increased proportions of mature relative to immature neurons consistent with reduced neurogenesis.
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