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PGC‐1 isoforms modulate the antioxidant response of photoreceptors to photo‐oxidative stress
Author(s) -
Iacovelli Jared,
Arany Zoltan,
SaintGeniez Magali
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1086.10
Subject(s) - oxidative stress , reactive oxygen species , microbiology and biotechnology , mitochondrion , programmed cell death , antioxidant , biology , gene expression , oxidative phosphorylation , chemistry , apoptosis , biochemistry , gene
Photoreceptors (PRs) are sensitive to oxidative stress due high oxygen consumption, high levels of light irradiation, and outer segments abundant in readily oxidized poly‐unsaturated fatty acids. This study examines expression of peroxisome proliferator‐activated receptor‐gamma coactivator 1 α and β (PGC‐1α/β), regulators of cellular metabolism and antioxidant response, in retina and their role in PR oxidative stress response in vitro . Mouse retina PGC‐1α/β□expression was studied by in situ hybridization, immunofluorescence and qPCR. 661w, photoreceptor‐like cells, were exposed to bright light, and reactive oxygen species (ROS) and cell death were analyzed. Knock‐down of PGC‐1α/β was performed using siRNA. PGC‐1α/β and antioxidant enzyme gene expression was analyzed by qPCR. PGC‐1α/β□expression increased during postnatal retinal development in mice, coinciding with increased mitochondrial gene expression. Bright light exposure increased ROS, up‐regulated PGC‐1α expression, and following prolonged exposure, caused cell death. Increased PGC‐1α/β expression may regulate the mitochondria burst associated with postnatal PR development. The photo‐oxidative stress induced increase in PGC‐1α levels and increased cell death following PGC‐1α/β knock‐down implies a role for PGC‐1α/β in PR antioxidant response. Funding was from T32‐ EY007035 ‐30 (JI) and Schepens “Start‐up” package (MSG).