Key result
Poliovirus simultaneously activates the PI3K/Akt survival signaling pathway in IMR5 neuroblastoma cells, which limits the extent of JNK activation and subsequent cell death.
The PI3K/Akt survival pathway may limit the spread of poliovirus-induced damage in the central nervous system by restricting JNK-mediated apoptosis.
PI3K/Akt may restrict poliovirus neuronal death; leaves open whether pathway modulation alters CNS infection outcomes.
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.
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Autret et al. (2008) studied Poliovirus infection. Poliovirus infection was evaluated on PI3K/Akt pathway activation and JNK-mediated cell death. Poliovirus simultaneously activates the PI3K/Akt survival signaling pathway in IMR5 neuroblastoma cells, which limits the extent of JNK activation and subsequent cell death.
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