| First Author | Ruiz-Palmero I | Year | 2013 |
| Journal | Mol Cell Endocrinol | Volume | 372 |
| Issue | 1-2 | Pages | 105-15 |
| PubMed ID | 23545157 | Mgi Jnum | J:201283 |
| Mgi Id | MGI:5512928 | Doi | 10.1016/j.mce.2013.03.018 |
| Citation | Ruiz-Palmero I, et al. (2013) G protein-coupled estrogen receptor is required for the neuritogenic mechanism of 17beta-estradiol in developing hippocampal neurons. Mol Cell Endocrinol 372(1-2):105-15 |
| abstractText | 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 (17beta-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. |
