Abstract
Purpose: :
To determine whether the ER stress-mediated apoptosis signal-regulating kinase 1 (ASK1)-c-Jun N-terminal kinase (JNK) pathway is associated with the degeneration of the retinal neurons induced by ischemia-reperfusion injury.
Methods: :
The rat retinal ischemia-reperfusion model was used. After 60 minutes of ischemia, the retinas were isolated and fixed after 6, 9, 12, 18, 24 hours, 2, 5 and 9 days of reperfusion. Cryosections were immunostained with Fluoro-Jade B, a degenerating neuron marker. Semi-quantitative analysis of the expression of IRE1α, ASK1, SAPK/ERK kinase 1 (SEK1), and JNK were performed in both control and ischemic retinas.
Results: :
In ischemic retinas, the intensities of IRE1α immunoreactivity in the ganglion cell layer (GCL) were significantly increased compared to those in the control retinas. In ischemic retinas, the numbers of SEK1-, ASK1-, and JNK-positive cells were significantly higher in the GCL compared to those in the control retinas. The cells that were positive for SEK1-, ASK1-, and JNK were also positive for Fluoro-Jade B-positive cells.
Conclusions: :
These results indicate that the ASK1-JNK pathway induced by ER stress was associated with the neuronal cell death after ischemia-reperfusion injury in rat retinas.
Keywords: retina • stress response • retinal degenerations: cell biology