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
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / physiology*
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Blotting, Western
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Calcium / metabolism*
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Cell Fractionation
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Cell Line, Tumor
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Cytosol / metabolism
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Endoplasmic Reticulum / metabolism*
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Flow Cytometry
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Humans
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Inositol 1,4,5-Trisphosphate Receptors / metabolism
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Mitochondria / metabolism*
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Mitochondrial Diseases / etiology*
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Poliomyelitis / complications*
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Poliomyelitis / metabolism
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Poliovirus*
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Ryanodine Receptor Calcium Release Channel / metabolism
Substances
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Inositol 1,4,5-Trisphosphate Receptors
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Ryanodine Receptor Calcium Release Channel
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Calcium