Chapter title |
JNK Inhibition Reduced Retinal Ganglion Cell Death after Ischemia/Reperfusion In Vivo and after Hypoxia In Vitro.
|
---|---|
Chapter number | 90 |
Book title |
Retinal Degenerative Diseases
|
Published in |
Advances in experimental medicine and biology, January 2016
|
DOI | 10.1007/978-3-319-17121-0_90 |
Pubmed ID | |
Book ISBNs |
978-3-31-917120-3, 978-3-31-917121-0
|
Authors |
Produit-Zengaffinen, Nathalie, Favez, Tatiana, Pournaras, Constantin J, Schorderet, Daniel F, Nathalie Produit-Zengaffinen, Tatiana Favez, Constantin J. Pournaras, Daniel F. Schorderet, Pournaras, Constantin J., Schorderet, Daniel F. |
Abstract |
Mitogen-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. |
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