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N. Hata, T. Oshitari, A. Yokoyama, Y. Mitamura, S. Yamamoto; Endoplasmic Reticulum Stress Is Associated With Retinal Neuronal Cell Death Induced by Ischemia-Reperfusion Injury. Invest. Ophthalmol. Vis. Sci. 2008;49(13):6119.
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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.
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.
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.
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.
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