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dc.contributor.authorPrieto, Ignacioes_ES
dc.contributor.authorZambrano, Albertoes_ES
dc.contributor.authorLaso, Javieres_ES
dc.contributor.authorAranda, Anaes_ES
dc.contributor.authorSamper, Enriquees_ES
dc.contributor.authorMonsalve, Maríaes_ES
dc.date.accessioned2019-08-21T11:54:39Z-
dc.date.available2019-08-21T11:54:39Z-
dc.date.issued2019-
dc.identifier.citationFree Radical Biology and Medicine 138: 23-32 (2019)es_ES
dc.identifier.issn0891-5849-
dc.identifier.urihttp://hdl.handle.net/10261/188750-
dc.description.abstract[Aims]: Oxidative stress is known to induce early replicative senescence. Senescence has been proposed to work as a barrier to immortalization and tumor development. Here, we aimed to evaluate the impact of the loss of peroxisome proliferator activated receptor γ co-activator 1α (PGC-1α), a master regulator of oxidative metabolism and mitochondrial reactive oxygen species (ROS) generation, on replicative senescence and immortalization in mouse embryonic fibroblasts (MEFs).es_ES
dc.description.abstract[Results]: We found that primary MEFs lacking PGC-1α showed higher levels of ROS than wild-type MEFs at all cell passages tested. The elevated production of ROS was associated with higher levels of oxidative DNA damage and the increased formation of DNA double-strand breaks. Evaluation of the induction of DNA repair systems in response to γ-radiation indicated that the loss of PGC-1α also resulted in a small but significant reduction in their activity. DNA damage induced the early activation of senescence markers, including an increase in the number of β-galactosidase-positive cells, the induction of p53 phosphorylation, and the increase in p16 and p19 protein. These changes were, however, not sufficient to reduce proliferation rates of PGC-1α-deficient MEFs at any cell passage tested. Moreover, PGC-1α-deficient cells escaped replicative senescence.es_ES
dc.description.abstract[Innovation & conclusion]: PGC-1α plays an important role in the control of cellular senescence and immortalization.es_ES
dc.description.sponsorshipThis work was supported by grants from the Spanish Ministerio de Economía Industria y Competitividad (MINEICO) and FEDER funds [Grant numbers SAF2012-37693, SAF2015-63904-R, SAF2015-71521-REDC, to M.M., BFU-2014-53610-P to A.A.], from the European Union's Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie Action grant agreement 721236-TREATMENT to M.M. and MPY-1038/14 and MPY-1146/16 from ISCIII to A.Z.es_ES
dc.language.isoenges_ES
dc.publisherElsevieres_ES
dc.relationMINECO/ICTI2013-2016/SAF2015-63904-Res_ES
dc.relationMINECO/ICTI2013-2016/SAF2015-71521-REDCes_ES
dc.relationMINECO/ICTI2013-2016/BFU-2014-53610-Pes_ES
dc.relationinfo:eu-repo/grantAgreement/EC/H2020/721236es_ES
dc.relation.isversionofPostprint-
dc.rightsembargoedAccesses_ES
dc.titleEarly induction of senescence and immortalization in PGC-1α-deficient mouse embryonic fibroblastses_ES
dc.typeartículoes_ES
dc.identifier.doi10.1016/j.freeradbiomed.2019.04.015-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1016/j.freeradbiomed.2019.04.015es_ES
dc.identifier.e-issn1873-4596-
dc.contributor.funderMinisterio de Economía, Industria y Competitividad (España)es_ES
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderEuropean Commissiones_ES
dc.contributor.funderInstituto de Salud Carlos IIIes_ES
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100010198es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.pmid31029787-
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