Tian, BoMaidana, DanielDib, BernardMiller, JohnBouzika, PeggyMiller, JoanVavvas, DemetriosLin, Haijiang2016-10-112016Tian, Bo, Daniel E. Maidana, Bernard Dib, John B. Miller, Peggy Bouzika, Joan W. Miller, Demetrios G. Vavvas, and Haijiang Lin. 2016. “miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.” PLoS ONE 11 (8): e0160887. doi:10.1371/journal.pone.0160887. http://dx.doi.org/10.1371/journal.pone.0160887.1932-6203http://nrs.harvard.edu/urn-3:HUL.InstRepos:29002607Oxidative stress has been shown to contribute to the development of age-related macular degeneration (AMD). MicroRNAs (miRNA) are small non-coding RNA molecules that function in RNA silencing and post-transcriptional regulation of gene expression. We showed miR-17-3p to be elevated in macular RPE cells from AMD patients and in ARPE-19 cells under oxidative stress. Transfection of miR-17-3p mimic in ARPE-19 induced cell death and exacerbated oxidative lethality that was alleviated by miR-17-3p inhibitor. The expression of antioxidant enzymes manganese superoxide dismutase (MnSOD) and thioredoxin reductase-2 (TrxR2) were suppressed by miR-17-3p mimic and reversed by miR-17-3p inhibitor. These results suggest miR-17-3p aggravates oxidative damage-induced cell death in human RPE cells, while miR-17-3p inhibitor acts as a potential protector against oxidative stress by regulating the expression of antioxidant enzymes.en-USBiology and Life SciencesCell BiologyOxidative StressBiochemistryAntioxidantsMolecular BiologyMolecular Biology TechniquesTransfectionBiology and life sciencesGeneticsGene expressionGene regulationMicroRNAsNucleic acidsRNANon-coding RNACell ProcessesCell DeathMedicine and Health SciencesGeriatricsGeriatric OphthalmologyMacular DegenerationOphthalmologyRetinal DisordersMacular DisordersRetinal DegenerationEnzymologyEnzyme ChemistryEnzyme RegulationAnatomyHeadEyesOcular SystemJournal Article2016-10-1110.1371/journal.pone.0160887