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dc.contributor.authorALVAREZ-FLORES, Miryam
hal.structure.identifierDepartment of Physiology
dc.contributor.authorHÉBERT, Audrey
dc.contributor.authorGOUELLE, Cathy
hal.structure.identifierPhysiologie de la reproduction et des comportements [Nouzilly] [PRC]
dc.contributor.authorGELLER, Sarah
hal.structure.identifierInstituto Butantan [São Paulo]
dc.contributor.authorCHUDZINSKI-TAVASSI, Ana
hal.structure.identifierUniversité de Lausanne = University of Lausanne [UNIL]
dc.contributor.authorPELLERIN, Luc
dc.date.accessioned2021-10-07T16:28:55Z
dc.date.available2021-10-07T16:28:55Z
dc.date.issued2019-01
dc.identifier.issn0022-3042
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/112621
dc.description.abstractEnThe recombinant Lonomia obliqua Stuart-factor activator (rLosac) is a recombinant hemolin which belongs to the immunoglobulin superfamily of cell adhesion molecules. It is capable of inducing pro-survival activity in serum-deprived human umbilical vein endothelial cells (HUVECs) and fibrob-lasts by increasing mitochondrial metabolism. We hypothesize that it could promote neuronal survival by acting on neuroen-ergetics. Our study reveals that treatment of primary mouse cortical neurons cultured in neurobasal medium lacking B27 supplement with rLosac led to an enhancement of cell viability in a time-and concentration-dependent manner. In parallel, preserved or enhanced phosphorylation of Akt, p44, and p42 MAPK, as well as mTOR was observed following treatment with rLosac. During deprivation, as assessed by western blot and qRT-PCR, protein and mRNA expression of MCT2 (the predominant neuronal monocarboxylate transporter allowing lactate use as an alternative energy substrate) decreased significantly in B27 supplement-deprived cortical neurons and was hardly detected after 24 h of deprivation. Interestingly, rLosac maintained MCT2 protein expression after 24 h of deprivation including at the cell surface without preventing mRNA loss. MCT2 knockdown reduced rLosac-enhanced cell viability, confirming its involvement in rLosac effect. Enhanced uptake of lactate was detected following rLosac treatment and might contribute to rLosac-enhanced viability during deprivation. In the presence of both lactate and rLosac, cell viability was higher than in the presence of lactate alone. Our observations suggest that rLosac promotes cell viability in stressed (B27 supplement-deprived) neurons by facilitating the use of lactate as energy substrate via the preservation of MCT2 protein expression.
dc.language.isoen
dc.publisherWiley
dc.subject.enneuroprotection
dc.subject.enrLosac
dc.subject.enenergy
dc.subject.enhemolin
dc.subject.enlactate
dc.subject.enMCT2
dc.title.enNeuroprotective effect of rLosac on supplement-deprived mouse cultured cortical neurons involves maintenance of monocarboxylate transporter MCT2 protein levels
dc.typeArticle de revue
dc.identifier.doi10.1111/jnc.14617
dc.subject.halSciences du Vivant [q-bio]
bordeaux.journalJournal of Neurochemistry
bordeaux.page80-96
bordeaux.volume148
bordeaux.hal.laboratoriesCentre de Résonance Magnétique des Systèmes Biologiques (CRMSB) - UMR 5536*
bordeaux.issue1
bordeaux.institutionUniversité de Bordeaux
bordeaux.institutionCNRS
bordeaux.peerReviewedoui
hal.identifierhal-02472310
hal.version1
hal.origin.linkhttps://hal.archives-ouvertes.fr//hal-02472310v1
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