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Estradiol activates PI3K/Akt/GSK3 pathway under chronic neurodegenerative conditions triggered by perinatal asphyxia

dc.contributor.authorSaraceno G.E.
dc.contributor.authorBellini M.J.
dc.contributor.authorGarcia-Segura L.M.
dc.contributor.authorCapani F.
dc.date.accessioned2020-09-02T22:28:06Z
dc.date.available2020-09-02T22:28:06Z
dc.date.issued2018
dc.identifier10.3389/fphar.2018.00335
dc.identifier.citation9, APR, -
dc.identifier.issn16639812
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6201
dc.descriptionPerinatal asphyxia (PA) remains as one of the most important causes of short-term mortality, psychiatric and neurological disorders in children, without an effective treatment. In previous studies we have observed that the expression of different neurodegenerative markers increases in CA1 hippocampal area of 4-months-old male rats born by cesarean section and exposed for 19 min to PA. We have also shown that a late treatment with 17β estradiol (daily dose of 250 μg/kg for 3 days) was able to revert the brain alterations observed in those animals. Based on these previous results, the main aim of the present study was to explore the mechanism by which the estrogenic treatment is involved in the reversion of the chronic neurodegenerative conditions induced by PA. We demonstrated that estradiol treatment of adult PA exposed animals induced an increase in estrogen receptor (ER) a and insulin-like growth factor receptor (IGF-1R) protein levels, an activation of the phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase 3 beta/β-catenin signaling pathway and an increase in Bcl-2/Bax ratio in the hippocampus in comparison to PA exposed animals treated with vehicle. Taking together, our data suggest that the interaction between ERa and IGF-IR, with the subsequent downstream activation, underlies the beneficial effects of estradiol observed in late treatment of PA. © 2018 Saraceno, Bellini, Garcia-Segura and Capani.
dc.language.isoen
dc.publisherFrontiers Media S.A.
dc.subjectHippocampus
dc.subjectNeuronal survival
dc.subjectNeuroprotection
dc.subjectSignaling pathway
dc.subjectWestern blot
dc.subjectbeta catenin
dc.subjectestradiol
dc.subjectestrogen receptor alpha
dc.subjectglycogen synthase kinase 3
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprotein Bax
dc.subjectprotein bcl 2
dc.subjectprotein kinase B
dc.subjectsomatomedin C receptor
dc.subjectadult
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectcontrolled study
dc.subjectdegenerative disease
dc.subjectdown regulation
dc.subjectdrug effect
dc.subjectdrug mechanism
dc.subjectenzyme activation
dc.subjectfemale
dc.subjecthippocampal CA1 region
dc.subjectmale
dc.subjectnerve cell plasticity
dc.subjectneuromodulation
dc.subjectneuroprotection
dc.subjectnonhuman
dc.subjectperinatal asphyxia
dc.subjectprotein protein interaction
dc.subjectrat
dc.subjectsignal transduction
dc.titleEstradiol activates PI3K/Akt/GSK3 pathway under chronic neurodegenerative conditions triggered by perinatal asphyxia
dc.typeArticle


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