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Cerebroprotective effect of 17β-Estradiol replacement therapy in ovariectomy-induced post-menopausal rats subjected to Ischemic Stroke : Role of MAPK/ERK1/2 pathway and PI3K-independent Akt activation

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Cerebroprotective effect of 17β-Estradiol replacement therapy in ovariectomy-induced post-menopausal rats subjected to Ischemic Stroke : Role of MAPK/ERK1/2 pathway and PI3K-independent Akt activation

dc.contributor.author	Burguete López, María Consuelo
dc.contributor.author	Jover Mengual, Teresa
dc.contributor.author	Castelló Ruiz, María
dc.contributor.author	López Morales, Mikahela Andrea
dc.contributor.author	Centeno Guil, José M.
dc.contributor.author	Aliena Valero, Alicia
dc.contributor.author	Alborch Domínguez, Enrique
dc.contributor.author	Torregrosa Bernabé, Germán
dc.contributor.author	Salom Sanvalero, Juan B.
dc.date.accessioned	2023-10-10T18:15:23Z
dc.date.available	2023-10-10T18:15:23Z
dc.date.issued	2023
dc.identifier.citation	Burguete López, María Consuelo Jover Mengual, Teresa Castelló Ruiz, María López Morales, Mikahela Andrea Centeno Guil, José M. Aliena Valero, Alicia Alborch Domínguez, Enrique Torregrosa Bernabé, Germán Salom Sanvalero, Juan B. 2023 Cerebroprotective effect of 17β-Estradiol replacement therapy in ovariectomy-induced post-menopausal rats subjected to Ischemic Stroke : Role of MAPK/ERK1/2 pathway and PI3K-independent Akt activation International Journal Of Molecular Sciences 24 18 14303
dc.identifier.uri	https://hdl.handle.net/10550/90090
dc.description.abstract	Despite the overwhelming advances in the understanding of the pathogenesis of stroke, a devastating disease affecting millions of people worldwide, currently there are only a limited number of effective treatments available. Preclinical and clinical studies show that stroke is a sexually dimorphic disorder, affecting males and females differently. Strong experimental evidence indicates that estrogen may play a role in this difference and that exogenous 17β-estradiol (E2) is neuroprotective against stroke in both male and female rodents. However, the molecular mechanisms by which E2 intervenes in ischemia-induced cell death, revealing these sex differences, remain unclear. The present study was aimed to determine, in female rats, the molecular mechanisms of two well-known pro-survival signaling pathways, MAPK/ERK1/2 and PI3K/Akt, that mediate E2 neuroprotection in response to acute ischemic stroke. E2 pretreatment reduced brain damage and attenuated apoptotic cell death in ovariectomized female rats after an ischemic insult. Moreover, E2 decreased phosphorylation of ERK1/2 and prevented ischemia/reperfusion-induced dephosphorylation of both Akt and the pro-apoptotic protein, BAD. However, MAPK/ERK1/2 inhibitor PD98059, but not the PI3K inhibitor LY294002, attenuated E2 neuroprotection. Thus, these results suggested that E2 pretreatment in ovariectomized female rats modulates MAPK/ERK1/2 and activates Akt independently of PI3K to promote cerebroprotection in ischemic stroke. A better understanding of the mechanisms and the influence of E2 in the female sex paves the way for the design of future successful hormone replacement therapies.
dc.language.iso	eng
dc.relation.ispartof	International Journal Of Molecular Sciences, 2023, vol. 24, num. 18, p. 14303
dc.subject	Malalties cerebrovasculars
dc.title	Cerebroprotective effect of 17β-Estradiol replacement therapy in ovariectomy-induced post-menopausal rats subjected to Ischemic Stroke : Role of MAPK/ERK1/2 pathway and PI3K-independent Akt activation
dc.type	journal article
dc.date.updated	2023-10-10T18:15:24Z
dc.identifier.doi	10.3390/ijms241814303
dc.identifier.idgrec	161280
dc.rights.accessRights	open access