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
PLOS ONE | 2016年 / 11卷 / 08期
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.
引用
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页数:15
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