Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10926243 | Cell Calcium | 2014 | 13 Pages |
Abstract
The mitochondrial permeability transition pore (mPTP) has long been known to have a role in mitochondrial calcium (Ca2+) homeostasis under pathological conditions as a mediator of the mitochondrial permeability transition and the activation of the consequent cell death mechanism. However, its role in the context of mitochondrial Ca2+ homeostasis is not yet clear. Several studies that were based on PPIF inhibition or knock out suggested that mPTP is involved in the Ca2+ efflux mechanism, while other observations have revealed the opposite result.The c subunit of the mitochondrial F1/FO ATP synthase has been recently found to be a fundamental component of the mPTP. In this work, we focused on the contribution of the mPTP in the Ca2+ efflux mechanism by modulating the expression of the c subunit. We observed that forcing mPTP opening or closing did not impair mitochondrial Ca2+ efflux. Therefore, our results strongly suggest that the mPTP does not participate in mitochondrial Ca2+ homeostasis in a physiological context in HeLa cells.
Keywords
ATP5G1ppifCyclosporine A (CsA)PICTSPOMCUANTRURMPTNCLXVDACMPTPsiRNAs[Ca2+]c[Ca2+]mHydrogen peroxidemitochondrial permeability transitionmitochondrial permeability transition poreCSAadenine nucleotide translocaseruthenium redCyclosporine Acytosolic calcium concentrationMitochondrial Ca2+ uniporterMitochondriahexokinase IIH2O2peptidyl prolyl isomerasevoltage-dependent anion channelCalcium (Ca2+)peripheral benzodiazepine receptor
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Authors
Elena De Marchi, Massimo Bonora, Carlotta Giorgi, Paolo Pinton,