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Glutamate‐evoked redox state alterations are involved in tissue transglutaminase upregulation in primary astrocyte cultures
Author(s) -
Campisi A.,
Caccamo D.,
Li Volti G.,
Currò M.,
Parisi G.,
Avola R.,
Vanella A.,
Ientile R.
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.10.074
Subject(s) - glutamate receptor , downregulation and upregulation , astrocyte , glutathione , oxidative stress , chemistry , cysteamine , intracellular , biochemistry , biology , endocrinology , receptor , central nervous system , enzyme , gene
The aim of this study was to evaluate the involvement of oxidative stress in glutamate‐evoked transglutaminase (TGase) upregulation in astrocyte cultures (14 DIV). A 24 h exposure to glutamate caused a dose‐dependent depletion of glutathione intracellular content and increased the ROS production in cell cultures. These effects were receptor‐mediated, as demonstrated by inhibition with GYKI 52466. The pre‐incubation with glutathione ethyl ester or cysteamine recovered oxidative status and was effective in significantly reducing glutamate‐increased tissue TGase. These data suggest that tissue TGase upregulation may be part of a biochemical response to oxidative stress induced by a prolonged exposure of astrocyte cultures to glutamate.