Produit-Zengaffinen, NathalieFavez, TatianaPournaras, Constantin J.Schorderet, Daniel F.2016-04-012016-04-012016-04-01201610.1007/978-3-319-17121-0_90https://infoscience.epfl.ch/handle/20.500.14299/125482WOS:000369715400090Mitogen-activated protein kinases (MAPKs) are key regulators that have been linked to cell survival and death. Among the main classes of MAPKs, c-jun N-terminal kinase (JNK) has been shown to mediate cell stress responses associated with apoptosis. In Vitro, hypoxia induced a significant increase in 661W cell death that paralleled increased activity of JNK and c-jun. 661W cells cultured in presence of the inhibitor of JNK (D-JNKi) were less sensitive to hypoxia-induced cell death. In vivo, elevation in intraocular pressure (IOP) in the rat promoted cell death that correlated with modulation of JNK activation. In vivo inhibition of JNK activation with D-JNKi resulted in a significant and sustained decrease in apoptosis in the ganglion cell layer, the inner nuclear layer and the photoreceptor layer. These results highlight the protective effect of D-JNKi in ischemia/reperfusion induced cell death of the retina.In vivoIschemiaHypoxiaMAPKJNKTherapytext::conference output::conference proceedings::conference paper