Failure to activate NF-κB promotes apoptosis of retinal ganglion cells following optic nerve transection

Abstract

NF-κB is a transcription factor, which is activated by various stimuli. One of the well-known activators of NF-κB is oxidative stress, which is a cause of cell death in some tissue, or cell types. Optic nerve transection, axotomy, results in retinal cell death, because of oxidative stress, deprivation of neurotrophic factors, etc. Since it has been hypothesized that the retinal ganglion cell death after axotomy is due to the generation of reactive oxygen species, we investigated whether NF-κB is involved in the retinal cell death after axotomy. This study was performed to investigate the role of NF-κB in retinal ganglion cell death after optic nerve transection. We used double staining experiment by using anti-NF-κB antibody and ethidium bromide to observe the correlation of NF-κB activation and the cell death. NF-κB was observed only in the surviving cells. NF-κB translocation was observed 3 days after the optic nerve transection. The NF-κB inhibitor, sulfasalazine, was used to block the activation of NF-κB in the axotomized retina, and the number of ganglion cells was quantified using retrograde in the presence or absence of sulfasalazine after axotomy. Inhibition of NF-κB by sulfasalazine accelerated the degeneration of ganglion cells in the retina. The results suggest that the activated NF-κB plays a protective role from the cell death in the injured ganglion cells.