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miR-17-3p Exacerbates Oxidative Damage in Human Retinal Pigment Epithelial Cells
被引:24
|作者:
Tian, Bo
[1
,2
]
Maidana, Daniel E.
[1
]
Dib, Bernard
[1
]
Miller, John B.
[1
]
Bouzika, Peggy
[1
]
Miller, Joan W.
[1
]
Vavvas, Demetrios G.
[1
]
Lin, Haijiang
[1
]
机构:
[1] Harvard Med Sch, Massachusetts Eye & Ear Infirm, Retina Serv, Angiogenesis Lab,Dept Ophthalmol, Boston, MA 02115 USA
[2] Zhengzhou Univ, Affiliated Hosp 1, Dept Ophthalmol, Zhengzhou, Henan, Peoples R China
来源:
关键词:
MITOCHONDRIAL SUPEROXIDE-DISMUTASE;
GENE-EXPRESSION;
DOWN-REGULATION;
MOUSE MODEL;
STRESS;
THIOREDOXIN;
ANTIOXIDANT;
LIGHT;
SOD2;
PHAGOCYTOSIS;
D O I:
10.1371/journal.pone.0160887
中图分类号:
O [数理科学和化学];
P [天文学、地球科学];
Q [生物科学];
N [自然科学总论];
学科分类号:
07 ;
0710 ;
09 ;
摘要:
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 (TrxR(2)) 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.
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页数:15
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