TY - JOUR
T1 - Le tranforming growth factor-beta (TGF-beta) a t-il un rôle neuroprotecteur dans l'ischémie cérébrale?
AU - Docagne, Fabian
AU - Ali, Carine
AU - Lesne, Sylvain
AU - Nicole, Olivier
AU - MacKenzie, Eric T.
AU - Buisson, Alain
AU - Vivien, Denis
PY - 2003
Y1 - 2003
N2 - Necrosis and apoptosis are the two fundamental hallmarks of neuronal death in stroke. Nevertheless, thrombolysis, by means of the recombinant serine protease t-PA, remains until now the only approved treatment of stroke in man. Over the last years, the cytokine termed Transforming Growth Factor-beta 1 (TGF-beta 1) has been found to be strongly up regulated in the central nervous system following ischemia-induced brain damage. Recent studies have shown a neuroprotective activity of TGF-beta 1 against ischemia-induced neuronal death. In vitro, TGF-beta 1 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. Altogether, these observations suggest that either TGF-beta signaling or TGF-beta 1-modulated genes could be good targets for the development of new therapeutic strategies for stroke in man.
AB - Necrosis and apoptosis are the two fundamental hallmarks of neuronal death in stroke. Nevertheless, thrombolysis, by means of the recombinant serine protease t-PA, remains until now the only approved treatment of stroke in man. Over the last years, the cytokine termed Transforming Growth Factor-beta 1 (TGF-beta 1) has been found to be strongly up regulated in the central nervous system following ischemia-induced brain damage. Recent studies have shown a neuroprotective activity of TGF-beta 1 against ischemia-induced neuronal death. In vitro, TGF-beta 1 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. Altogether, these observations suggest that either TGF-beta signaling or TGF-beta 1-modulated genes could be good targets for the development of new therapeutic strategies for stroke in man.
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U2 - 10.1051/jbio/2003197020145
DO - 10.1051/jbio/2003197020145
M3 - Review article
C2 - 12910629
AN - SCOPUS:0142122078
SN - 1295-0661
VL - 197
SP - 145
EP - 150
JO - Journal de la Société de biologie
JF - Journal de la Société de biologie
IS - 2
ER -
