Insulin-like growth factor-I receptors and estrogen receptors interact in the promotion of neuronal survival and neuroprotection

被引:83
作者
Garcia-Segura, LM [1 ]
Cardona-Gómez, GP
Chowen, LA
Azcoitia, I
机构
[1] CSIC, Inst Cajal, E-28002 Madrid, Spain
[2] Hosp Nino Jesus, Unidad Invest, E-28009 Madrid, Spain
[3] Univ Complutense Madrid, Fac Biol, Dept Biol Celular, E-28040 Madrid, Spain
来源
JOURNAL OF NEUROCYTOLOGY | 2000年 / 29卷 / 5-6期
关键词
D O I
10.1023/A:1007125626308
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Several in vitro and in vivo studies have shown that estrogen has neuroprotective properties. The neuroprotective effects of estrogen are probably exerted through several mechanisms, it is established that estrogen can provide neuroprotection by actions that are independent of estrogen receptor activation. In addition, in several experimental models, activation of estrogen receptors appears to be indispensable for neuroprotection. This review focuses on neuroprotection mediated by estrogen receptors. The interaction of estrogen with growth factor receptor signaling to induce neuroprotection is discussed. Evidence is presented that estrogen receptors and insulin-like growth factor-I receptors interact in the promotion of neuronal survival and neuroprotection.
引用
收藏
页码:425 / 437
页数:13
相关论文
共 130 条
[61]   Peptide growth factor cross-talk with the estrogen receptor requires the A/B domain and occurs independently of protein kinase C or estradiol [J].
IgnarTrowbridge, DM ;
Pimentel, M ;
Parker, MG ;
McLachlan, JA ;
Korach, KS .
ENDOCRINOLOGY, 1996, 137 (05) :1735-1744
[62]   INSULIN-LIKE GROWTH-FACTORS AND THEIR BINDING-PROTEINS - BIOLOGICAL ACTIONS [J].
JONES, JI ;
CLEMMONS, DR .
ENDOCRINE REVIEWS, 1995, 16 (01) :3-34
[63]  
Jordan CL, 1999, J NEUROBIOL, V40, P434, DOI 10.1002/(SICI)1097-4695(19990915)40:4<434::AID-NEU2>3.0.CO
[64]  
2-T
[65]   Systemic administration of kainic acid induces selective time dependent decrease in [I-125]insulin-like growth factor I, [I-125]insulin-like growth factor II and [I-125]insulin receptor binding sites in adult rat hippocampal formation [J].
Kar, S ;
Seto, D ;
Dore, S ;
Chabot, JG ;
Quirion, R .
NEUROSCIENCE, 1997, 80 (04) :1041-1055
[66]   ACTIVATION OF THE ESTROGEN-RECEPTOR THROUGH PHOSPHORYLATION BY MITOGEN-ACTIVATED PROTEIN-KINASE [J].
KATO, S ;
ENDOH, H ;
MASUHIRO, Y ;
KITAMOTO, T ;
UCHIYAMA, S ;
SASAKI, H ;
MASUSHIGE, S ;
GOTOH, Y ;
NISHIDA, E ;
KAWASHIMA, H ;
METZGER, D ;
CHAMBON, P .
SCIENCE, 1995, 270 (5241) :1491-1494
[67]   Insulin-like growth factor-I protects axotomized rat retinal ganglion cells from secondary death via PI3-K-dependent akt phosphorylation and inhibition of caspase-3 in vivo [J].
Kermer, P ;
Klöcker, N ;
Labes, M ;
Bähr, M .
JOURNAL OF NEUROSCIENCE, 2000, 20 (02) :722-728
[68]   Cloning of a novel estrogen receptor expressed in rat prostate and ovary [J].
Kuiper, GGJM ;
Enmark, E ;
PeltoHuikko, M ;
Nilsson, S ;
Gustafsson, JA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (12) :5925-5930
[69]   The estrogen receptor β subtype:: A novel mediator of estrogen action in neuroendocrine systems [J].
Kuiper, GGJM ;
Shughrue, PJ ;
Merchenthaler, I ;
Gustafsson, JA .
FRONTIERS IN NEUROENDOCRINOLOGY, 1998, 19 (04) :253-286
[70]   The endocrinology of aging [J].
Lamberts, SWJ ;
vandenBeld, AW ;
vanderLely, AJ .
SCIENCE, 1997, 278 (5337) :419-424