Autotaxin protects microglial cells against oxidative stress

Abstract : Oxidative stress occurs when antioxidant defenses are overwhelmed by oxygen-reactive species and can lead to cellular damage, as seen in several neurodegenerative disorders. Microglia are specialized cells in the central nervous system that act as the first and main form of active immune defense in the response to pathological events. Autotaxin (ATX) plays an important role in the modulation of critical cellular functions, through its enzymatic production of lysophosphatidic acid (LPA). In this study, we investigated the potential role of ATX in the response of microglial cells to oxidative stress. We show that treatment of a microglial BV2 cell line with hydrogen peroxide (H2O2) stimulates ATX expression and LPA production. Stable overexpression of ATX inhibits microglial activation (CD11b expression) and protects against H2O2-treatment-induced cellular damage. This protective effect of ATX was partially reduced in the presence of the LPA-receptor antagonist Ki16425. ATX overexpression was also associated with a reduction in intracellular ROS formation, carbonylated protein accumulation, proteasomal activity, and catalase expression. Our results suggest that up-regulation of ATX expression in microglia could be a mechanism for protection against oxidative stress, thereby reducing inflammation in the nervous system.
Type de document :
Article dans une revue
Free Radical Biology and Medicine, Elsevier, 2012, 52 (2), pp.516--526. 〈10.1016/j.freeradbiomed.2011.11.014〉
Liste complète des métadonnées

http://hal.univ-reunion.fr/hal-01198333
Contributeur : Nicolas Alarcon <>
Soumis le : vendredi 11 septembre 2015 - 21:06:16
Dernière modification le : dimanche 5 novembre 2017 - 15:58:06

Identifiants

Collections

Citation

Rana Awada, Philippe Rondeau, Sandra Grès, Jean Sébastien Saulnier-Blache, Christian Lefebvre d'Hellencourt, et al.. Autotaxin protects microglial cells against oxidative stress. Free Radical Biology and Medicine, Elsevier, 2012, 52 (2), pp.516--526. 〈10.1016/j.freeradbiomed.2011.11.014〉. 〈hal-01198333〉

Partager

Métriques

Consultations de la notice

69