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. Epub 2010 Sep 22.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / physiology*
  • Blotting, Western
  • Calcium / metabolism*
  • Cell Fractionation
  • Cell Line, Tumor
  • Cytosol / metabolism
  • Endoplasmic Reticulum / metabolism*
  • Flow Cytometry
  • Humans
  • Inositol 1,4,5-Trisphosphate Receptors / metabolism
  • Mitochondria / metabolism*
  • Mitochondrial Diseases / etiology*
  • Poliomyelitis / complications*
  • Poliomyelitis / metabolism
  • Poliovirus*
  • Ryanodine Receptor Calcium Release Channel / metabolism

Substances

  • Inositol 1,4,5-Trisphosphate Receptors
  • Ryanodine Receptor Calcium Release Channel
  • Calcium