Exploring the Potential Role of the Oxidant-Activated Transcription Factor Aryl Hydrocarbon Receptor in the Pathogenesis of AMD
Cigarette smoking is the most consistently shown risk factor associated with progression of all forms of age-related macular degeneration. The signaling pathways activated by cigarette smoke oxidants have not been fully elucidated. Herein, we review the effect of oxidant injury in retinal pigment epithelial cells at the subcellular level, introduce an oxidant-activated transcription factor called aryl hydrocarbon receptor, and discuss mechanisms by which this receptor may regulate the oxidative stress response in RPE cells and disease.
KeywordsAge-related macular degeneration Oxidative stress Retinal pigment epithelium Mitochondria Aryl hydrocarbon receptor
This work was supported by a grant from the American Health Assistance Foundation (GM) and Research to Prevent Blindness.
- Alcazar O, Hawkridge AM, Collier TS et al (2009) Proteomic characterization of cell membrane blebs in human retinal pigment epithelium cells. Mol Cell ProteomicsGoogle Scholar
- Diani-Moore S, Papachristou F, Labitzke E, Rifkind AB (2006) Induction of CYP1A and cyp2-mediated arachidonic acid epoxygenation and suppression of 20-hydroxyeicosatetraenoic acid by imidazole derivatives including the aromatase inhibitor vorozole. Drug Metab Dispos 34:1376–1385PubMedCrossRefGoogle Scholar
- Marin-Castano ME, Striker GE, Alcazar O, Catanuto P, Espinosa-Heidmann DG, Cousins SW (2006) Repetitive nonlethal oxidant injury to retinal pigment epithelium decreased extracellular matrix turnover in vitro and induced sub-RPE deposits in vivo. Invest Ophthalmol Vis Sci 47:4098–4112PubMedCrossRefGoogle Scholar