An Up-regulation of IRF-1 After a Spinal Cord Injury: Implications for Neuronal Apoptosis

J Mol Neurosci. 2015 Dec;57(4):595-604. doi: 10.1007/s12031-015-0642-2. Epub 2015 Sep 5.

Abstract

IRF-1, a kind of transcription factor, is expressed in many cell types, except in early embryonal cells. IRF-1 has played an essential role in various physiological and pathological processes, including tumor immune surveillance, viral infection, development of immunity system and pro-inflammatory injury. However, the expression and function of IRF-1 in spinal cord injury (SCI) are still unknown. In this study, we have performed an acute SCI model in adult rats and investigated the dynamic changes of IRF-1 expression in the spinal cord. Western blot have shown that IRF-1 protein levels gradually increased, reaching a peak at day 3 and then gradually declined to a normal level at day 14 after SCI. Double immunofluorescence staining showed that IRF-1 immunoreactivity was found in neurons, but not in astrocytes and microglia. Additionally, colocalization of IRF-1/active caspase-3 was detected in neurons. In vitro, IRF-1 depletion, by short interfering RNA, obviously decreases neuronal apoptosis. In conclusion, this is the first description of IRF-1 expression in spinal cord injury. Our results suggested that IRF-1 might play crucial roles in CNS pathophysiology after SCI.

Keywords: Apoptosis; Interferon regulatory factor 1; Neuron; Spinal cord injury.

MeSH terms

  • Animals
  • Apoptosis*
  • Astrocytes / metabolism
  • Cells, Cultured
  • Interferon Regulatory Factor-1 / genetics
  • Interferon Regulatory Factor-1 / metabolism*
  • Male
  • Neurons / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Spinal Cord Injuries / metabolism*
  • Up-Regulation

Substances

  • Interferon Regulatory Factor-1
  • Irf1 protein, rat