Transforming growth factor-β and ischemic brain injury

被引：84

作者：

Alain Buisson ^{[1
]}

Sylvain Lesne ^{[1
]}

Fabian Docagne ^{[1
]}

Carine Ali ^{[1
]}

Olivier Nicole ^{[1
]}

Eric T. MacKenzie ^{[1
]}

Denis Vivien ^{[1
]}

机构：

[1] Université de CAEN, UMR CNRS 6551, Centre CYCERON, Caen Cedex, bd H. Becquerel

[2] Universite de CAEN-CNRS UMR 6551, Centre CYCERON, IFR 47

来源：

Cellular and Molecular Neurobiology | 2003年 / 23卷 / 4-5期

关键词：

Cerebral ischemia; Molecular; TGF-β;

D O I：

10.1023/A:1025072013107

中图分类号：

学科分类号：

摘要：

1. Necrosis and apoptosis are the two fundamental hallmarks of neuronal death in stroke. Nevertheless, thrombolysis, by using the recombinant serine protease t-PA, remains until now the only approved treatment of stroke in man. 2. Over the last years, the cytokine termed Transforming Growth Factor-β1 (TGF-β1) has been found to be strongly up-regulated in the central nervous system following ischemia-induced brain damage. 3. Recent studies have shown a neuroprotective activity of TGF-β1 against ischemia-induced neuronal death. In vitro, TGF-β1 protects neurons against excitotoxicity by inhibiting the t-PA-potentiated NMDA-induced neuronal death through a mechanism involving the up-regulation of the type-1 plasminogen activator inhibitor (PAI-1) in astrocytes. 4. In addition, TGF-β1 has been recently characterized as an antiapoptotic factor in a model of staurosporine-induced neuronal death through a mechanism involving activation of the extracellular signal-regulated kinase 1/2 (Erk1/2) and a concomitant increase phosphorylation of the antiapoptotic protein Bad. 5. Altogether, these observations suggest that either TGF-β signaling or TGF-β1-modulated genes could be good targets for the development of new therapeutic strategies for stroke in man.

引用

页码：539 / 550

页数：11

共 53 条

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