Increased nuclear factor-κB p65 immunoreactivity following retinal ischemia and reperfusion injury in mice

Yue guo Chen, Cheng Zhang, Samuel K.S. Chiang, Tinghuai Wu, Mark O.M. Tso

Research output: Contribution to journalArticle

34 Scopus citations


Nuclear factor-κB (NF-κB) is a universal transcription factor and has previously been demonstrated to play an important role in CNS injury. This study investigated the expression of NF-κB in the inner layers of the retina in mice after retinal ischemia and reperfusion injury. Retinal ischemia was induced by elevation of intraocular pressure to 120 mmHg for 60 min. To evaluate inner retinal degeneration, the inner retinal thickness was quantified with an image-analysis system. The inner retinal thickness increased in the initial 24 hr after retinal ischemia and was ascribed to tissue edema but was significantly decreased in the ensuing 7 days. Immunohistochemistry using NF-κB p65 monoclonal antibody was performed on the retina and was corelated with TUNEL labeling. Six hours after retinal ischemia, nuclear p65 immunoreactivity was increased in the inner nuclear and ganglion cell layers and reached a peak at 24 hr. The increased NF-κB p65 immunolabeling was parallel to the TUNEL labeling. Double labeling with p65 and TUNEL showed partial colocalization of p65 and TUNEL labeling in the scattered cells of the inner nuclear and ganglion cell layers. However, several p65-positive cells were TUNEL negative, suggesting that these cells might have survived the injury. The NF-κB p65 immunoreactivity was associated with retinal degeneration following retinal ischemia and reperfusion injury.

Original languageEnglish (US)
Pages (from-to)125-131
Number of pages7
JournalJournal of Neuroscience Research
Issue number1
Publication statusPublished - Apr 1 2003
Externally publishedYes



  • Immunohistochemistry
  • Ischemia and reperfusion
  • Mice
  • NF-κB
  • Retina

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

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