Calcium flux between the endoplasmic reticulum and mitochondrion contributes to poliovirus-induced apoptosis

  • J Virol. 2010 Dec;84(23):12226-35. doi: 10.1128/JVI.00994-10.
Cynthia Brisac  1 ,  François Téoulé ,  Arnaud Autret ,  Isabelle Pelletier ,  Florence Colbère-Garapin ,  Catherine Brenner ,  Christophe Lemaire ,  Bruno Blondel
Affiliations
  • 1. Institut Pasteur, Unité de Biologie des Virus Entériques, 25 rue du Dr Roux, Paris, France.
PMID: 20861253 DOI: 10.1128/JVI.00994-10
Abstract

We show that poliovirus (PV) Infection induces an increase in cytosolic calcium (CA(2+)) concentration in neuroblastoma IMR5 cells, at least partly through CA(2+) release from the endoplasmic reticulum lumen via the inositol 1,4,5-triphosphate receptor (IP(3)R) and ryanodine receptor (RyR) channels. This leads to CA(2+) accumulation in mitochondria through the mitochondrial CA(2+) uniporter and the voltage-dependent anion channel (VDAC). This increase in mitochondrial CA(2+) concentration in PV-infected cells leads to mitochondrial dysfunction and Apoptosis.

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