视网膜
糖尿病性视网膜病变
视网膜色素上皮
视网膜
增殖性玻璃体视网膜病变
基因表达
下调和上调
分子生物学
基因
细胞培养
细胞生长
作者
Ying Li,Ting Cheng,Chengliang Wan,Yanhong Cang
出处
期刊:Gene
[Elsevier]
日期:2020-07-15
卷期号:747: 144653-
被引量:19
标识
DOI:10.1016/j.gene.2020.144653
摘要
Diabetic retinopathy (DR) is a frequent complication of diabetes and it can lead to visual impairment and blindness. However, the mechanism of their regulation remains little known. circRNAs can function as crucial competing endogenous RNA, which can sponge corresponding miRNAs and affect mRNA expression in various diseases, including DR. In our current research, we observed that circRNA_0084043 was elevated in high glucose (HG)-incubated ARPE-19 cells. Then, we focused on whether and how circRNA_0084043 participated in retinal vascular dysfunction under conditions diabetes. Apoptosis, inflammation and oxidative stress are hallmark of DR progression. This work was aimed to investigate the signaling mechanisms of circRNA_0084043 in these pathogenesis of DR. We discovered loss of circRNA_0084043 significantly increased cell survival and repressed HG-triggered apoptosis. In addition, knockdown of circRNA_0084043 remarkably reduced oxidative stress as evidenced by the down-regulated malondialdehyde (MDA) content, enhanced activities of Super Oxide Dismutase (SOD) and Glutathione peroxidase (GSH-PX). Addition, silence of circRNA_0084043 effectively restrained HG-stimulated inflammation as proved by repressing inflammatory cytokines Tumor Necrosis Factor α (TNF-α), Interleukin 6 (IL-6) and Cox-2 in ARPE-19 cells. Subsequently, we successfully predicted that miR-140-3p was a downstream target of circRNA_0084043, which could be negatively regulated by circRNA_0084043. Mechanistically, loss of miR-140-3p abrogated the beneficial effects of circRNA_0084043 siRNA on ARPE-19 cells. Transforming Growth Factor alpha (TGFA) can exhibit a role in multiple diseases. Taken these together, these data demonstrated that loss of circRNA_0084043 depressed HG-induced damage via sponging miR-140-3p and regulating TGFA.
科研通智能强力驱动
Strongly Powered by AbleSci AI