MicroRNA Regulation for Inflammasomes in High Glucose-Treated ARPE-19 Cells

被引:1
|
作者
Kim, Ji Hong [1 ,2 ]
Yu, Hyoseon [1 ]
Kang, Ji Hye [1 ]
Hong, Eun Hee [1 ,3 ,4 ]
Kang, Min Ho [1 ,3 ]
Seong, Mincheol [1 ,3 ,5 ]
Cho, Heeyoon [1 ,3 ,5 ]
Shin, Yong Un [1 ,3 ,4 ]
机构
[1] Hanyang Univ, Coll Med, Dept Ophthalmol, Seoul, South Korea
[2] Hanyang Univ, Seoul Hosp, Dept Ophthalmol, Seoul, South Korea
[3] Hanyang Univ, Guri Hosp, Dept Ophthalmol, Guri, Gyeonggi Do, South Korea
[4] Hanyang Univ, Hanyang Inst Biosci & Biotechnol, Seoul, South Korea
[5] NOON Eye Clin, Guri, Gyeonggi Do, South Korea
基金
新加坡国家研究基金会;
关键词
THIOREDOXIN-INTERACTING PROTEIN; NLRP3; INFLAMMASOME; ACTIVATION;
D O I
10.1155/2024/3654690
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Purpose. This study aimed to evaluate the expression of microRNAs (miRNAs) and inflammasomes in diabetes-induced retinal cells and to determine their role in the pathogenesis of diabetic retinopathy (DR). Methods. To establish diabetes-induced cell models, ARPE-19 cells were treated with high glucose. The expression levels of five miRNAs (miR-185, miR-17, miR-20a, miR-15a, and miR-15b) were measured in high glucose-treated ARPE-19 cells using real-time quantitative polymerase chain reaction. Western blotting was performed to measure inflammasome expression in cellular models. miR-17 was selected as the target miRNA, and inflammasome expression was measured following the transfection of an miR-17 mimic into high glucose-treated ARPE-19 cells. Results. In high glucose-treated ARPE-19 cells, miRNA expression was substantially downregulated, whereas that of inflammasome components was significantly increased. Following the transfection of the miR-17 mimic into high glucose-treated ARPE-19 cells, the levels of inflammasome components were significantly decreased. Conclusions. This study investigated the relationship between miRNAs and inflammasomes in diabetes-induced cells using high glucose-treated ARPE-19 cells. These findings suggested that miR-17 suppresses inflammasomes, thereby reducing the subsequent inflammatory response and indicating that miRNAs and inflammasomes could serve as new therapeutic targets for DR.
引用
收藏
页数:7
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