Upregulation of D site of albumin promoter binding protein in the brain of patients with intractable epilepsy

Mol Med Rep. 2015 Apr;11(4):2486-92. doi: 10.3892/mmr.2014.3065. Epub 2014 Dec 9.

Abstract

The mechanisms that underlie the pathogenesis of intractable epilepsy (IE) remain to be elucidated. The present study aimed to investigate the expression of D site of albumin promoter binding protein (DBP) and mitogen‑activated protein kinases (MAPKs) in the temporal lobes of patients with IE, in order to examine the possible roles of DBP in the pathogenesis of IE. The expression of DBP and MAPK was detected by immunohistochemistry and double‑label immunofluorescence staining against DBP/MAPK in 35 patients with IE, and the data were compared with those of the 15 controls. The results demonstrated that DBP expression in IE group (0.31±0.03) was significantly higher compared with that in the controls (0.18±0.02; P<0.05) and MAPK expression in the IE group (0.19±0.03) was also higher compared with that in the controls (0.12±0.02; P<0.05). DBP and MAPK were mainly expressed in the cytoplasm of neurons and the double‑label immunofluorescence staining demonstrated that DBP and MAPK expression occurred in the same neurons. Therefore, the expression of DBP and MAPK in epilepsy patients was upregulated, suggesting a possible pathogenetic role in IE.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Brain / metabolism*
  • Case-Control Studies
  • Child
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Epilepsy / genetics*
  • Epilepsy / metabolism
  • Female
  • Gene Expression Regulation*
  • Humans
  • Immunohistochemistry
  • Male
  • Middle Aged
  • Mitogen-Activated Protein Kinases / metabolism
  • Neocortex / metabolism
  • Temporal Lobe / metabolism
  • Transcription Factors / genetics*
  • Transcription Factors / metabolism
  • Up-Regulation
  • Young Adult

Substances

  • DBP protein, human
  • DNA-Binding Proteins
  • Transcription Factors
  • Mitogen-Activated Protein Kinases