Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10883143 | Mitochondrion | 2012 | 6 Pages |
Abstract
Phosphate activation of the mitochondrial permeability transition pore (MPTP) opening is well-documented and could involve the phosphate carrier (PiC) that we have proposed is the pore's cyclophilin-D binding component. However, others have reported that following CyP-D ablation Pi inhibits MPTP opening while cyclosporine-A (CsA) inhibits MPTP opening only when Pi is present. Here we demonstrate that Pi activates MPTP opening under all energised and de-energised conditions tested while CsA inhibits pore opening whether or not Pi is present. Using siRNA in HeLa cells we could reduce PiC expression by 65-80% but this inhibited neither mitochondrial calcium accumulation nor MPTP opening.
Keywords
NTAMPTPMPTSFAANTBKAPICVDACCATPPIaseCyP-DPeptidyl-prolyl cis-trans isomeraseOMMCarboxyatractylosideSanglifehrin ACyclophilin-DROSReperfusion injuryBongkrekic acidnitrilotriacetic acidPermeability transition poremitochondrial permeability transitionmitochondrial permeability transition poreimmCSAadenine nucleotide translocasemitochondrial phosphate carrierinner mitochondrial membraneCyclosporine Acalcium retention capacityouter mitochondrial membranePhosphateHeartPoly(ethylene glycol)PEGCRCCalciumReactive oxygen species
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Authors
Pinadda Varanyuwatana, Andrew P. Halestrap,