Role of serum TRAIL level and TRAIL apoptosis gene expression in multiple sclerosis and relation to brain atrophy

J Clin Neurosci. 2014 Sep;21(9):1606-11. doi: 10.1016/j.jocn.2013.11.056. Epub 2014 Jun 7.

Abstract

One of the presumed pathological mechanisms of multiple sclerosis (MS) is the failure of apoptosis of autoreactive T lymphocytes. This study aimed to determine the relationship of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mRNA gene expression ratio and serum TRAIL levels with MS and brain atrophy. This study was conducted on 53 relapsing-remitting Egyptian MS patients and 25 matched healthy volunteers. The expression of TRAIL in peripheral blood lymphocytes was analyzed by reverse transcription polymerase chain reaction, serum levels of soluble TRAIL (sTRAIL) were determined by enzyme-linked immunosorbent assay and brain MRI measured "black holes" and the bicaudate ratio as a measure of brain atrophy in all patients. The serum TRAIL level was lower in MS patients compared to controls but no difference was seen in the TRAIL mRNA gene expression ratio. No significant correlation was detected between the serum TRAIL level and the TRAIL mRNA expression ratio in either group. No statistically significant correlation was found between serum TRAIL levels or the TRAIL mRNA expression ratio with the number of black holes or the bicaudate ratio on MRI. Apoptosis of T lymphocytes is decreased in MS patients, which could be useful when designing treatments. There was no difference in the TRAIL mRNA gene expression ratio between MS patients and controls.

Keywords: Apoptosis; Multiple sclerosis; TRAIL mRNA gene expression; Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).

MeSH terms

  • Adult
  • Atrophy
  • Brain / pathology*
  • Case-Control Studies
  • Egypt
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Gene Expression
  • Humans
  • Lymphocytes / metabolism
  • Magnetic Resonance Imaging
  • Male
  • Multiple Sclerosis, Relapsing-Remitting / metabolism*
  • Multiple Sclerosis, Relapsing-Remitting / pathology*
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • TNF-Related Apoptosis-Inducing Ligand / metabolism*

Substances

  • RNA, Messenger
  • TNF-Related Apoptosis-Inducing Ligand
  • TNFSF10 protein, human