Molecular mechanisms involved in the regulation of neuritogenesis by estradiol: Recent advances

被引:45
作者
Angeles Arevalo, Maria [1 ]
Ruiz-Palmero, Isabel [1 ]
Julia Scerbo, Maria [2 ]
Acaz-Fonseca, Estefania [1 ]
Julia Cambiasso, Maria [2 ]
Garcia-Segura, Luis M. [1 ]
机构
[1] CSIC, Inst Cajal, E-28002 Madrid, Spain
[2] IMMF CONICET, Lab Neurofisiol, RA-5000 Cordoba, Argentina
关键词
Brain derived neurotrophic factor; Estrogen receptors; G-protein-coupled-receptor; 30; Insulin-like growth factor-I; Mitogen activated protein kinase; Neurogenin; 3; Phosphoinositide-3; kinase; GROWTH-FACTOR-I; HIPPOCAMPAL ESTROGEN SYNTHESIS; RAT HYPOTHALAMIC NEURONS; DEVELOPING PURKINJE-CELL; ADULT SENSORY NEURONS; NEURITE GROWTH; RESPONSE-ELEMENT; NEUROTROPHIC FACTOR; NEURAL DEVELOPMENT; SIGNALING PATHWAY;
D O I
10.1016/j.jsbmb.2011.09.004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
This review analyzes the signaling mechanisms activated by estradiol to regulate neuritogenesis in several neuronal populations. Estradiol regulates axogenesis by the activation of the mitogen activated protein kinase (MAPK) cascade through estrogen receptor a located in the plasma membrane. In addition, estradiol regulates MAPK signaling via the activation of protein kinase C and by increasing the expression of brain derived neurotrophic factor and tyrosine kinase receptor B. Estradiol also interacts with the signaling of insulin-like growth factor-I receptor through estrogen receptor alpha, modulating the phosphoinositide-3 kinase signaling pathway, which contributes to the stabilization of microtubules. Finally, estradiol modulates dendritogenesis by the inhibition of Notch signaling, by a mechanism that, at least in hippocampal neurons, is mediated by G-protein coupled receptor 30. This article is part of a Special Issue entitled 'Neurosteroids'. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:52 / 56
页数:5
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