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Título: | G protein-coupled estrogen receptor is required for the neuritogenic mechanism of 17β-estradiol in developing hippocampal neurons |
Autor: | Ruiz-Palmero, Isabel CSIC; Hernando, M.; García-Segura, Luis M. CSIC ORCID; Arévalo, María Ángeles CSIC ORCID | Palabras clave: | Hes1 Cerebellin 4 Amyloid β Hippocampus NGF Alzheimer's disease |
Fecha de publicación: | 2013 | Editor: | Elsevier | Citación: | Molecular and Cellular Endocrinology 372: 105- 115 (2013) | Resumen: | Estradiol promotes neuritogenesis in developing hippocampal neurons by a mechanism involving the upregulation of neurogenin 3, a Notch-regulated transcription factor. In this study we have explored whether G-protein coupled estrogen receptor 1 (GPER) participates in this hormonal action. GPER agonists (17β-estradiol, G1, ICI 182,780) increased neurogenin 3 expression and neuritogenesis in mouse primary hippocampal neurons and this effect was blocked by the GPER antagonist G15 and by a siRNA for GPER. In addition, GPER agonists increased Akt phosphorylation in ser473, which is indicative of the activation of phosphoinositide-3-kinase (PI3K). G15 or GPER silencing prevented the estrogenic induction of Akt phosphorylation. Furthermore, the PI3K inhibitor wortmannin prevented the effect of G1 and estradiol on neurogenin 3 expression and the effect of estradiol on neuritogenesis. These findings suggest that GPER participates in the control of hippocampal neuritogenesis by a mechanism involving the activation of PI3K signaling. © 2013 Elsevier Ireland Ltd. | URI: | http://hdl.handle.net/10261/150280 | DOI: | 10.1016/j.mce.2013.03.018 | Identificadores: | doi: 10.1016/j.mce.2013.03.018 issn: 0303-7207 |
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