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dc.contributor.authorBlasco Angulo, Natividad
dc.contributor.authorBeà Tàrrega, Aida
dc.contributor.authorBarés Junqué, Gisel
dc.contributor.authorGirón, Cristina
dc.contributor.authorNavaridas Fernández de Bobadilla, Raúl
dc.contributor.authorIrazoki, Andrea
dc.contributor.authorLópez-Lluch, Guillermo
dc.contributor.authorZorzano, Antonio
dc.contributor.authorDolcet Roca, Xavier
dc.contributor.authorLlovera i Tomàs, Marta
dc.contributor.authorSanchis, Daniel
dc.date.accessioned2021-03-04T09:40:52Z
dc.date.available2021-03-04T09:40:52Z
dc.date.issued2020-10-05
dc.identifier.issn2213-2317
dc.identifier.urihttp://hdl.handle.net/10459.1/70681
dc.description.abstractThe apoptotic nuclease EndoG is involved in mitochondrial DNA replication. Previous results suggested that, in addition to regulate cardiomyocyte hypertrophy, EndoG could be involved in cell proliferation. Here, by using in vivo and cell culture models, we investigated the role of EndoG in cell proliferation. Genetic deletion of Endog both in vivo and in cultured cells or Endog silencing in vitro induced a defect in rodent and human cell proliferation with a tendency of cells to accumulate in the G1 phase of cell cycle and increased reactive oxygen species (ROS) production. The defect in cell proliferation occurred with a decrease in the activity of the AKT/PKB-GSK-3β-Cyclin D axis and was reversed by addition of ROS scavengers. EndoG deficiency did not affect the expression of ROS detoxifying enzymes, nor the expression of the electron transport chain complexes and oxygen consumption rate. Addition of the micropeptide Humanin to EndoG-deficient cells restored AKT phosphorylation and proliferation without lowering ROS levels. Thus, our results show that EndoG is important for cell proliferation through the control of ROS and that Humanin can restore cell division in EndoG-deficient cells and counteracts the effects of ROS on AKT phosphorylation.
dc.description.sponsorshipThis research was funded by Ministerio de Ciencia e Innovación, Gobierno de España, grant numbers SAF2013-44942-R and PID2019-104509RB-I00 to D.S. and SAF2016-80157-R to X.D.; Fundació La Marató, Catalunya, grant number 20153810 to D.S.; AGAUR, Generalitat de Catalunya, Catalunya, grant number 2014-SGR-1609 to D.S. G.B. holds a contract from the University of Lleida; A.B. contract has been funded by Fundació La Marató TV3 and Diputació de Lleida/IRBLleida.
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.publisherElsevier
dc.relationMINECO/PN2013-2016/SAF2013-44942-R
dc.relationMINECO/PN2017-2020/PID2019-104509RB-I00
dc.relationMINECO/PN2013-2016/SAF2016-80157-R
dc.relation.isformatofReproducció del document publicat a: https://doi.org/10.1016/j.redox.2020.101736
dc.relation.ispartofRedox Biology, 2020, vol. 37, p. 101736
dc.rightscc-by-nc-nd (c) Blasco Angulo, Natividad et al., 2020
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectEndoG
dc.subjectCell proliferation
dc.subjectMitochondria
dc.subjectReactive oxygen species
dc.subjectCell signaling
dc.subjectHumanin
dc.subjectRomo1
dc.titleInvolvement of the mitochondrial nuclease EndoG in the regulation of cell proliferation through the control of reactive oxygen species
dc.typeinfo:eu-repo/semantics/article
dc.date.updated2021-03-04T09:40:52Z
dc.identifier.idgrec030472
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.identifier.doihttps://doi.org/10.1016/j.redox.2020.101736


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cc-by-nc-nd (c) Blasco Angulo, Natividad et al., 2020
Except where otherwise noted, this item's license is described as cc-by-nc-nd (c) Blasco Angulo, Natividad et al., 2020