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

NF-kappaB is a transcription factor, which is activated by various stimuli. One of the well-known activators of NF-kappaB is oxidative stress, which i s a cause of cell death in some tissue, or cell types. Optic nerve transect ion, axotomy, results in retinal cell death, because of oxidative stress, d eprivation of neurotrophic factors, etc. Since it has been hypothesized tha t the retinal ganglion cell death after axotomy is due to the generation of reactive oxygen species, we investigated whether NF-kappaB is involved in the retinal cell death after axotomy. This study was performed to investiga te the role of NF-kappaB in retinal ganglion cell death after optic nerve t ransection. We used double staining experiment by using anti-NF-kappaB anti body and ethidium bromide to observe the correlation of NF-kappaB activatio n and the cell death. NF-kappaB was observed only in the surviving cells. N F-kappaB translocation was observed 3 days after the optic nerve transectio n. The NF-kappaB inhibitor, sulfasalazine, was used to block the activation of NF-kappaB in the axotomized retina, and the number of ganglion cells wa s quantified using retrograde in the presence or absence of sulfasalazine a fter axotomy. Inhibition of NF-kappaB by sulfasalazine accelerated the dege neration of ganglion cells in the retina. The results suggest that the acti vated NF-kappaB plays a protective role from the cell death in the injured ganglion cells. (C) 2000 Elsevier Science B.V. All rights reserved.