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H.-C. H. Wang, H. D. Yarbrough, D. R. Clarkson, S. T. Schuschereba, B. E. Stuck; NF-B Activation in Laser-Induced Retinal Injury in Rabbits. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4406.
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NF-ΚB is a ubiquitous transcription factor, acts as a master regulator of stress response in a variety of conditions, and plays a pivotal role in cell injury. This study is to investigate the role of NF-ΚB in laser-induced retinal injury in rabbits.
Rabbits were exposed to a multiline argon laser (454 to 514) to produce lesions on the retina and euthanized at 1 h to 24 h post injury. The lesions on the rabbit retina were examined in hematoxylin and eosin-stained sections at 1, 3, 8 and 24 h after laser exposure by light microscopy. The active NF-ΚB p65 immunoreactivity at lesions was studied by immunohistochemistry. Neutrophil infiltration to the lesions was identified by a specific antibody to NP-5 with immunohistochemistry. The effects of the laser to induce photoreceptor apoptosis was determined by TUNEL.
Morphologic study of the retina after exposure to argon laser showed disrupted retinal pigment epithelium (RPE) and pyknotic photoreceptors at the lesion sites. The time course of neutrophil entry into retinal and choroidal compartment indicated that a peak at 8 h after laser exposure. The immunohistochemical data showed that perinuclear region of the Outer Nucleus Layer (ONL) was heavily labeled with an antibody to activated NF-ΚB at 1 h after injury. Nuclear localization of NF-ΚB in the ONL was seen at 3, 8, 24 h after injury. The nuclear transcolation of active NF-ΚB was identified in the nuclei of pyknotic photoreceptors. Furthermore, TUNEL stain revealed apoptotic photoreceptors at lesion sites which correlated with severity of the lesions.
Laser exposure to retina induced the NF-ΚB activation in the photoreceptor cells. The NF-ΚB activation exerts pro-apoptotic activity in laser-induced retinal injury.
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