Transforming growth factor-β signalling in brain disorders

被引：106
作者：
Vivien, D [1 ]
Ali, C [1 ]
机构：
[1] Univ Caen, Ctr CYCERON, INSERM, F-14074 Caen, France
来源：
CYTOKINE & GROWTH FACTOR REVIEWS | 2006年 / 17卷 / 1-2期
关键词：
transforming growth factor-beta; neuroprotection; ischemic stroke; Alzheimer's disease;
D O I：
10.1016/j.cytogfr.2005.09.011
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Transforming growth factor-beta (TGF-beta) has been characterized as an injury-related factor, based on the observation that it is strongly upregulated in many acute or chronic central nervous system disorders. TGF-beta is generally thought to be neuroprotective and several mechanisms have been proposed to explain this beneficial action. For instance, TGF-beta protects neurons against the potentiating effect of tissue-type plasminogen activator on NMDA receptor-mediated excitotoxicity, by up-regulating type-1 plasminogen activator inhibitor expression in astrocytes. TGF-beta has also anti-apoptotic properties, through a recruitment of a mitogen-activated protein kinase pathway and a concomitant activation of anti-apoptotic members of the Bcl-2 family. These multiple mechanisms might reflect the pleiotropic nature of TGF-beta, reinforcing the potential therapeutic value of this cytokine in several central nervous system disorders. (c) 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码：121 / 128
页数：8
相关论文
共 112 条
[1]   Increased expression of transforming growth factor-β after cerebral ischemia in the baboon:: An endogenous marker of neuronal stress? [J].
Ali, C ;
Docagne, F ;
Nicole, O ;
Lesné, S ;
Toutain, J ;
Young, A ;
Chazalviel, L ;
Divoux, D ;
Caly, M ;
Cabal, P ;
Derlon, JM ;
MacKenzie, ET ;
Buisson, A ;
Vivien, D .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2001, 21 (07) :820-827
[2]  
*AM HEART ASS, 2002, HEART DIS STROK STAT
[3]   TGF-β1, regulation of Alzheimer amyloid precursor protein mRNA expression in a normal human astrocyte cell line:: mRNA stabilization [J].
Amara, FM ;
Junaid, A ;
Clough, RR ;
Liang, BH .
MOLECULAR BRAIN RESEARCH, 1999, 71 (01) :42-49
[4]   β-Amyloid-induced glial expression of both pro- and anti-inflammatory cytokines in cerebral cortex of aged transgenic Tg2576 mice with Alzheimer plaque pathology [J].
Apelt, J ;
Schliebs, R .
BRAIN RESEARCH, 2001, 894 (01) :21-30
[5]   TRANSFORMING GROWTH-FACTOR-BETA ATTENUATES ISCHEMIA-INDUCED ALTERATIONS IN CEREBROVASCULAR RESPONSES [J].
ARMSTEAD, WM ;
MIRRO, R ;
ZUCKERMAN, SL ;
SHIBATA, M ;
LEFFLER, CW .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 264 (02) :H381-H385
[6]   Expression of various TGF-beta isoforms and type I receptor in necrotizing human brain lesions [J].
Ata, AK ;
Funa, K ;
Olsson, Y .
ACTA NEUROPATHOLOGICA, 1997, 93 (04) :326-333
[7]   Expression of transforming growth factor-β1, 2, 3 isoforms and type I and II receptors in acute focal cerebral ischemia:: an immunohistochemical study in rat after transient and permanent occlusion of middle cerebral artery [J].
Ata, KA ;
Lennmyr, F ;
Funa, K ;
Olsson, Y ;
Terént, A .
ACTA NEUROPATHOLOGICA, 1999, 97 (05) :447-455
[8]   TGFβ and Wnt pathway cross-talk [J].
Attisano, L ;
Labbé, E .
CANCER AND METASTASIS REVIEWS, 2004, 23 (1-2) :53-61
[9]   Mechanisms of disease:: Role of transforming growth factor β in human disease. [J].
Blobe, GC ;
Schiemann, WP ;
Lodish, HF .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (18) :1350-1358
[10]  
Bottner M, 1996, NEUROREPORT, V7, P2903
12345678910