Abstract：
:The mitochondrial permeability transition pore (mPTP) has long been known to have a role in mitochondrial calcium (Ca(2+)) 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 Ca(2+) homeostasis is not yet clear. Several studies that were based on PPIF inhibition or knock out suggested that mPTP is involved in the Ca(2+) 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 Ca(2+) efflux mechanism by modulating the expression of the c subunit. We observed that forcing mPTP opening or closing did not impair mitochondrial Ca(2+) efflux. Therefore, our results strongly suggest that the mPTP does not participate in mitochondrial Ca(2+) homeostasis in a physiological context in HeLa cells.
journal_name
Cell Calciumjournal_title
Cell calciumauthors
De Marchi E,Bonora M,Giorgi C,Pinton Pdoi
10.1016/j.ceca.2014.03.004subject
Has Abstractpub_date
2014-07-01 00:00:00pages
1-13issue
1eissn
0143-4160issn
1532-1991pii
S0143-4160(14)00053-0journal_volume
56pub_type
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