title: miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells.
abstract: Oxidative 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.
authors: Retina Service, Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America.|Department of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, P.R. China.
authors: Bo
authors: B
authors: Tian
authors: Retina Service, Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America.
authors: Daniel E
authors: DE
authors: Maidana
authors: Retina Service, Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America.
authors: Bernard
authors: B
authors: Dib
authors: Retina Service, Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America.
authors: John B
authors: JB
authors: Miller
authors: Retina Service, Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America.
authors: Peggy
authors: P
authors: Bouzika
authors: Retina Service, Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America.
authors: Joan W
authors: JW
authors: Miller
authors: Retina Service, Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America.
authors: Demetrios G
authors: DG
authors: Vavvas
authors: Retina Service, Angiogenesis Laboratory, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary, Harvard Medical School, Boston, MA, United States of America.
authors: Haijiang
authors: H
authors: Lin
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000975:Antioxidants / Q000378:metabolism; D002470:Cell Survival / Q000235:genetics; D015971:Gene Expression Regulation, Enzymologic / Q000235:genetics; D006801:Humans; D008268:Macular Degeneration / Q000235:genetics / Q000473:pathology; D035683:MicroRNAs / Q000235:genetics*; D018384:Oxidative Stress / Q000235:genetics*; D055213:Retinal Pigment Epithelium / Q000201:enzymology / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000378:metabolism; D054482:Thioredoxin Reductase 2 / Q000378:metabolism
chemical_list: D000975:Antioxidants; C524941:MIRN17 microRNA, human; D035683:MicroRNAs; D013482:Superoxide Dismutase; D054482:Thioredoxin Reductase 2