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C Zhang, Y Chen, SK S Chiang, TH Wu, MO M Tso; Nuclear Factor-kB Activation Following Retinal Ischemia and Reperfusion Injury in Mice . Invest. Ophthalmol. Vis. Sci. 2002;43(13):774.
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Purpose: Nuclear factor-kB (NF-kB), a universal transcription factor, has previously been demonstrated to play an important role in CNS ischemic injury. This study investigated the expression of NF-kB in inner retinal neurons following retinal ischemia and reperfusion injury in mice. Methods: Retinal ischemia was induced by transient elevation of intraocular pressure to 120 mmHg for 60 min. Inner retinal degeneration was quantified by an image analysis system. Immuno-histochemistry using NF-kB p65 monoclonal antibody was performed on the retina and co-related with TUNEL labeling. NF-kB p65 binding activity of the retinas was evaluated at different times post-ischemia by electrophoretic mobility gel shift assays (EMSA). Results: The inner retinal thickness was increased in the initial 24 h following ischemic injury and was ascribed to tissue edema, but was significantly decreased by day 7. Six hours after ischemia, nuclear p65 immunoreactivity was increased in the inner nuclear and ganglion cell layers, and reached a peak at 24 h, and was parallel to TUNEL labeling. Double labeling with p65 and TUNEL showed partial co-localization of p65 and TUNEL labeling predominantly in the inner nuclear layer. Delayed intense labeling of p65 was seen in retinal vasculature at 168 h after ischemia. EMSA showed that p65 binding activity remarkably decreased starting at 1 h after ischemia and persisted to 24 h, and recovered to normal basal levels at day 7 post-ischemia. Conclusion: NF-kB appeared to be activated and exhibited nuclear translocation in retinal degeneration after retinal ischemia and reperfusion injury. The pro- and anti- apoptotic effects of NF-kB and its pathway after retinal ischemia are being further investigated.
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