Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 473, Issue 4, Pages 1013-1018Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.04.008
Keywords
Retina; Light damage; NF-kappa B; Cytochrome C oxidase III
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan [24390393, 23659804]
- Translational Research Network Program [15lm0103007j0004]
- Program for the Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation [10-06]
- Grants-in-Aid for Scientific Research [23659804, 24390393, 16K15729, 16H05485] Funding Source: KAKEN
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The transcription factor nuclear factor kappaB (NF-kappa B) plays various roles in cell survival, apoptosis, and inflammation. In the rat retina, NF-kappa B activity increases after exposure to damaging light, resulting in degeneration of photoreceptors. Here, we report that in dark-adapted rats exposed for 6 h to bright white light, the p65 subunit of retinal NF-kappa B translocates to the mitochondria, an event associated with a decrease in expression of cytochrome c oxidase subunit III (COX III). However, sustained exposure for 12 h depleted p65 from the mitochondria, and enhanced COX III expression. Treatment with the protective antioxidant PBN prior to light exposure prevents p65 depletion in the mitochondria and COX III upregulation during prolonged exposure, and apoptosis in photoreceptor cells. These results indicate that COX III expression is sensitive to the abundance of NF-kappa B p65 in the mitochondria, which, in turn, is affected by exposure to damaging light. (C) 2016 Elsevier Inc. All rights reserved.
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