RIG-I knockdown impedes neurogenesis in a murine model of Japanese encephalitis

Cell Biol Int. 2015 Feb;39(2):224-9. doi: 10.1002/cbin.10354. Epub 2014 Aug 11.

Abstract

Retinoic acid inducible gene I (RIG-I) is a well established pattern recognition receptor (PRR) in neurons infected with Japanese encephalitis virus (JEV) as reported previously from our laboratory. Japanese encephalitis (JE) virus infection in brain has been shown to decrease the proliferation of neural stem/progenitor cells (NSPCs) which has its implications in neurological sequelae in JE survivors. We have found that ablation of RIG-I both in vivo and in vitro models results in significant decrease in NSPC proliferation post JEV infection. We hypothesize that knockdown of RIG-I diminishes the expression of antiviral molecules resulting in an increase in viral replication, which in turn results in enhancement of the expression of cell cycle inhibitors, hence affecting the proliferation of NSPCs.

Keywords: Japanese encephalitis virus; knockdown; morpholino; neural stem/progenitor cells (NSPC); neurogenesis; retinoic acid inducible gene I (RIG-I).

MeSH terms

  • Animals
  • Cells, Cultured
  • Disease Models, Animal
  • Encephalitis Virus, Japanese / physiology
  • Encephalitis, Japanese / pathology
  • Encephalitis, Japanese / veterinary
  • Encephalitis, Japanese / virology
  • Female
  • Male
  • Membrane Proteins / antagonists & inhibitors
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Mice
  • Mice, Inbred BALB C
  • Nerve Tissue Proteins / antagonists & inhibitors
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • Neural Stem Cells / cytology
  • Neural Stem Cells / metabolism
  • RNA Interference
  • RNA, Small Interfering / metabolism
  • Receptors, Cell Surface
  • Virus Replication

Substances

  • Membrane Proteins
  • Nerve Tissue Proteins
  • RNA, Small Interfering
  • Receptors, Cell Surface
  • Robo3 protein, mouse