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MicroRNA-34a promotes mitochondrial dysfunction-induced apoptosis in human lens epithelial cells by targeting Notch2 期刊论文

编号：

028e0e23-6716-40a4-b437-b17eb19869a2
作者：

Fan, Fan^[1,2,3];Zhuang, Jianhui^[4];Zhou, Peng^[5];Liu, Xin^[1,2,3];Luo, Yi(罗怡)*^[1,2,3]
语种：

English
期刊：

ONCOTARGET ISSN：1949-2553 2017 年 8 卷 66 期 (110209 - 110220) ; DEC 15
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关键词：

miR-34a HLECs apoptosis age-related cataract Notch
摘要：

Purpose: Human lens epithelial cell (HLEC) apoptosis is a common pathogenic mechanism in age-related cataracts (ARC). While the function of microRNAs (miRNAs) in the eye is beginning to be explored using miRNA expression array, the role of miR-34a in regulating HLEC apoptosis remains unknown and requires further investigation. Methods: Quantitative reverse-transcript polymerase chain reaction (RT-PCR) was used to determine the expression level of miR-34a in cataractous and control samples. MiR-34a mimics and small interfering RNAs were transfected into SRA01/04. Cell apoptosis and oxidative stress were assessed by flow cytometry. The Dual-Luciferase Reporter Assay System was used to confirm whether miR-34a bound to the 3'-UTR of the target gene and blocked its activity. The potential roles of the identified target genes in apoptosis and mitochondria dysfunction were also evaluated. Results: The expression of miR-34a increased in lens epithelial samples of ARC compared with the transparent group (cataract 2.41 +/- 0.81 vs. control 1.20 +/- 0.44, P=0.005). In cultured SRA01/04, miR-34a increased reactive oxygen species production and induced apoptosis (early apoptosis: 45.55%+/- 5.96% vs. 15.85%+/- 4.93%, P<0.01; late apoptosis: 6.10%+/- 2.67% vs. 0.95%+/- 0.42%, P<0.01). Overexpression of miR-34a promoted mitochondria-mediated apoptosis through activation of caspase-9, disruption of the mitochondrial membrane potential, blocking of mitochondrial energy metabolism and enhancement of cytochrome C release. Furthermore, Notch1 and Notch2 were confirmed as putative targets of miR-34a, but only Notch2 was verified as the effector that triggered mitochondria-mediated apoptosis. Conclusion: MicroRNA-34a is increased in the cataractous lens and triggers mitochondria-mediated apoptosis and oxidative stress by suppressing Notch2.
推荐引用方式
GB/T 7714：

Fan Fan,Zhuang Jianhui,Zhou Peng, et al. MicroRNA-34a promotes mitochondrial dysfunction-induced apoptosis in human lens epithelial cells by targeting Notch2 [J].ONCOTARGET,2017,8(66):110209-110220.
APA：

Fan Fan,Zhuang Jianhui,Zhou Peng,Liu Xin,&Luo Yi.(2017).MicroRNA-34a promotes mitochondrial dysfunction-induced apoptosis in human lens epithelial cells by targeting Notch2 .ONCOTARGET,8(66):110209-110220.
MLA：

Fan Fan, et al. "MicroRNA-34a promotes mitochondrial dysfunction-induced apoptosis in human lens epithelial cells by targeting Notch2" .ONCOTARGET 8,66(2017):110209-110220.

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