Journal
NEUROENDOCRINOLOGY
Volume 84, Issue 4, Pages 275-279Publisher
KARGER
DOI: 10.1159/000097485
Keywords
Akt; beta-catenin; estrogen receptors; glycogen synthase kinase 3; mitogen-activated protein kinase; phosphatidylinositol 3-kinase; tau
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The actions of estradiol in the brain involve the interaction with growth factors, such as insulin-like growth factor-I (IGF-I). Many cells in the brain coexpress receptors for estradiol (ERs) and IGF-I (IGF-IR) and both factors interact to regulate neural function. Several studies have shown that there is an interaction of IGF-IR and ERs in neuroprotection. Neuroprotective effects of estradiol are blocked by the inhibition of IGF-IR signaling, while the neuroprotective effects of IGF-I are blocked by the inhibition of ER signaling. These findings suggest that the neuroprotective actions of estradiol and IGF-I after brain injury depend on the coactivation of both ERs and IGF-IR in neural cells. The relationship of ER alpha with IGF-IR through the phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase 3 beta (PI3K/Akt/GSK3) signaling pathway may represent the point of convergence used by estradiol and IGF-I to cooperatively promote neuroprotection. Administration of estradiol to ovariectomized rats results in the association of ER alpha with IGF-IR and with components of the PI3K/Akt/GSK3 signaling pathway and in the regulation of the activity of Akt and GSK3 in the brain. Conversely, IGF-I regulates ER alpha transcriptional activity in neuroblastoma cells and the PI3K/Akt/GSK3 signaling pathway is involved in this effect. Copyright (c) 2006 S. Karger AG, Basel.
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