Early phosphatidylinositol 3-kinase/Akt pathway activation limits poliovirus-induced JNK-mediated cell death

J Virol. 2008 Apr;82(7):3796-802. doi: 10.1128/JVI.02020-07. Epub 2008 Jan 23.

Abstract

Poliovirus (PV)-induced apoptosis seems to play a major role in tissue injury in the central nervous system (CNS). We have previously shown that this process involves PV-induced Bax-dependent mitochondrial dysfunction mediated by early JNK activation in IMR5 neuroblastoma cells. We showed here that PV simultaneously activates the phosphatidylinositol 3-kinase (PI3K)/Akt survival signaling pathway in these cells, limiting the extent of JNK activation and thereby cell death. JNK inhibition is associated with PI3K-dependent negative regulation of the apoptosis signal-regulating kinase 1, which acts upstream from JNK in PV-infected IMR5 cells. In poliomyelitis, this survival pathway may limit the spread of PV-induced damage in the CNS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis*
  • Cell Line
  • Humans
  • MAP Kinase Kinase 4 / antagonists & inhibitors
  • MAP Kinase Kinase Kinase 5 / antagonists & inhibitors
  • Oncogene Protein v-akt / metabolism*
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Poliovirus / physiology*

Substances

  • Phosphatidylinositol 3-Kinases
  • Oncogene Protein v-akt
  • MAP Kinase Kinase Kinase 5
  • MAP Kinase Kinase 4