JNK Inhibition Reduced Retinal Ganglion Cell Death after Ischemia/Reperfusion In Vivo and after Hypoxia In Vitro

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.


Editor(s):
Rickman, Cb
Lavail, Mm
Anderson, Re
Grimm, C
Hollyfield, J
Ash, J
Published in:
Retinal Degenerative Diseases: Mechanisms And Experimental Therapy, 854, 677-683
Presented at:
16th International Symposium on Retinal Degeneration (RD), Pacific Grove, CA, JUL 13-18, 2014
Year:
2016
Publisher:
Cham, Springer Int Publishing Ag
ISSN:
0065-2598
ISBN:
978-3-319-17121-0
978-3-319-17120-3
Keywords:
Laboratories:




 Record created 2016-04-01, last modified 2018-05-09


Rate this document:

Rate this document:
1
2
3
 
(Not yet reviewed)