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Metastasis suppressor NM23 limits oxidative stress in mammals by preventing activation of stress‐activated protein kinases/JNKs through its nucleoside diphosphate kinase activity

dc.rights.licenseopenen_US
dc.contributor.authorPEUCHANT, Evelyne
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorBATS, Marie‐Lise
dc.contributor.authorMORANVILLIER, Isabelle
dc.contributor.authorLEPOIVRE, Michel
dc.contributor.authorGUITTON, Jérôme
dc.contributor.authorWENDUM, Dominique
dc.contributor.authorLACOMBE, Marie‐Lise
dc.contributor.authorMOREAU‐GAUDRY, François
dc.contributor.authorBOISSAN, Mathieu
dc.contributor.authorDABERNAT, Sandrine
dc.date.accessioned2020
dc.date.available2020
dc.date.issued2017
dc.identifier.issn0892-6638, 1530-6860en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/21227
dc.description.abstractEnAbstract NME1 (nonmetastatic expressed 1) gene, which encodes nucleoside diphosphate kinase (NDPK) A [also known as nonmetastatic clone 23 (NM23)-H1 in humans and NM23-M1 in mice], is a suppressor of metastasis, but several lines of evidence-mostly from plants-also implicate it in the regulation of the oxidative stress response. Here, our aim was to investigate the physiologic relevance of NDPK A with respect to the oxidative stress response in mammals and to study its molecular basis. NME1-knockout mice died sooner, suffered greater hepatocyte injury, and had lower superoxide dismutase activity than did wild-type (WT) mice in response to paraquat-induced acute oxidative stress. Deletion of NME1 reduced total NDPK activity and exacerbated activation of the stress-related MAPK, JNK, in the liver in response to paraquat. In a mouse transformed hepatocyte cell line and in primary cultures of normal human keratinocytes, MAPK activation in response to H2O2 and UVB, respectively, was dampened by expression of NM23-M1/NM23-H1, dependent on its NDPK catalytic activity. Furthermore, excess or depletion of NM23-M1/NM23-H1 NDPK activity did not affect the intracellular bulk concentration of nucleoside di- and triphosphates. NME1-deficient mouse embryo fibroblasts grew poorly in culture, were more sensitive to stress than WT fibroblasts, and did not immortalize, which suggested that they senesce earlier than do WT fibroblasts. Collectively, these results indicate that the NDPK activity of NM23-M1/NM23-H1 protects cells from acute oxidative stress by inhibiting activation of JNK in mammal models.-Peuchant, E., Bats, M.-L., Moranvillier, I., Lepoivre, M., Guitton, J., Wendum, D., Lacombe, M.-L., Moreau-Gaudry, F., Boissan, M., Dabernat, S. Metastasis suppressor NM23 limits oxidative stress in mammals by preventing activation of stress-activated protein kinases/JNKs through its nucleoside diphosphate kinase activity.
dc.language.isoENen_US
dc.subject*Article RECHERCHE
dc.title.enMetastasis suppressor NM23 limits oxidative stress in mammals by preventing activation of stress‐activated protein kinases/JNKs through its nucleoside diphosphate kinase activity
dc.typeArticle de revueen_US
dc.identifier.doi10.1096/fj.201600705Ren_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
bordeaux.journalThe FASEB Journalen_US
bordeaux.page1531–1546en_US
bordeaux.volume31en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires - U1034en_US
bordeaux.issue4en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
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