Oxidative stress induces mitochondrial dysfunction and a protective unfolded protein response in RPE cells

ABSTRACT: How retinal pigmented epithelial (RPE) cells degenerate from oxidative stress in age-related macular degeneration (AMD) is incompletely understood. The study's intent was to identify key cytoprotective pathways activated by oxidative stress, and to determine the extent of their protection. Immunohistochemistry was used to identify the unfolded protein response (UPR) and mitochondria in the RPE of AMD samples. Maculas with early AMD had prominent IRE1α, but minimal mitochondrial TOM20 immunolabeling in mildly degenerated RPE. RPE cells treated with cigarette smoke extract (CSE), by microarray analysis, had over-represented genes involved in the antioxidant and unfolded protein response, and mitochondrial location. CSE induced the UPR sensors IRE1α, p-PERK, and ATP6, which activated CHOP. CH

ORGANISM(S): Homo sapiens

SUBMITTER: Marisol Cano 

PROVIDER: E-GEOD-49107 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress