Induction of the permeability transition pore in cells depleted of mitochondrial DNA (Articolo in rivista)

Type
Label
  • Induction of the permeability transition pore in cells depleted of mitochondrial DNA (Articolo in rivista) (literal)
Anno
  • 2012-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1016/j.bbabio.2012.02.022 (literal)
Alternative label
  • Masgras, Ionica; Rasola, Andrea; Bernardi, Paolo (2012)
    Induction of the permeability transition pore in cells depleted of mitochondrial DNA
    in Biochimica et biophysica acta. Bioenergetics
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Masgras, Ionica; Rasola, Andrea; Bernardi, Paolo (literal)
Pagina inizio
  • 1860 (literal)
Pagina fine
  • 1866 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
  • http://www.ncbi.nlm.nih.gov/pubmed/22402226 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 1817 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
  • 7 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 10 (literal)
Note
  • ISI Web of Science (WOS) (literal)
  • Scopu (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Consiglio Nazionale delle Ricerche Institute of Neurosciences, University of Padova, Padova, Italy / Department of Biomedical Sciences, University of Padova, Padova, Italy (literal)
Titolo
  • Induction of the permeability transition pore in cells depleted of mitochondrial DNA (literal)
Abstract
  • Respiratory complexes are believed to play a role in the function of the mitochondrial permeability transition pore (PTP), whose dysregulation affects the process of cell death and is involved in a variety of diseases, including cancer and degenerative disorders. We investigated here the PTP in cells devoid of mitochondrial DNA (rho(0) cells), which lack respiration and constitute a model for the analysis of mitochondrial involvement in several pathological conditions. We observed that mitochondria of rho(0) cells maintain a membrane potential and that this is readily dissipated after displacement of hexokinase (HK) II from the mitochondrial surface by treatment with either the drug clotrimazole or with a cell-permeant HK II peptide, or by placing rho(0) cells in a medium without serum and glucose. The PTP inhibitor cyclosporin A (CsA) could decrease the mitochondrial depolarization induced by either HK II displacement or by nutrient depletion. We also found that a fraction of the kinases ERK1/2 and GSK3 alpha/beta is located in the mitochondrial matrix of rho(0) cells, and that glucose and serum deprivation caused concomitant ERK1/2 inhibition and GSK3 alpha/beta activation with the ensuing phosphorylation of cyclophilin D, the mitochondrial target of CsA. GSK3 alpha/beta inhibition with indirubin-3'-oxime decreased PTP-induced cell death in rho(0) cells following nutrient ablation. These findings indicate that rho(0) cells are equipped with a functioning PTP, whose regulatory mechanisms are similar to those observed in cancer cells, and suggest that escape from PTP opening is a survival factor in this model of mitochondrial diseases. This article is part of a Special Issue entitled: 17th European Bioenergetics Conference (EBEC 2012). (C) 2012 Elsevier B.V. All rights reserved. (literal)
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