Inhibition of miR-29a-3p Alleviates Apoptosis of Lens Epithelial Cells via Upregulation of CAND1

被引:1
作者
Fang, Rui [1 ]
Li, Hai-Long [2 ,3 ]
Lv, Ning-Xin [1 ]
Yue, Pei-Lin [1 ]
Jia, Yu-Xuan [1 ]
Liu, Zhao-Chuan [1 ,4 ,5 ]
Zhou, Hong-Gang [2 ,3 ,7 ]
Song, Xu-Dong [1 ,4 ,5 ,6 ]
机构
[1] Capital Med Univ, Beijing Tongren Hosp, Beijing, Peoples R China
[2] Nankai Univ, State Key Lab Med Chem Biol, Coll Pharm, Tianjin, Peoples R China
[3] Nankai Univ, Key Lab Mol Drug Res, Tianjin, Peoples R China
[4] Beijing Tongren Eye Ctr, Beijing, Peoples R China
[5] Beijing Ophthalmol & Visual Sci Key Lab, Beijing, Peoples R China
[6] Beijing Tongren Hosp, Beijing 100730, Peoples R China
[7] Nankai Univ, Tianjin 300071, Peoples R China
基金
中国国家自然科学基金;
关键词
miR-29a-3p; CAND1; apoptosis; lens epithelial cells; senile cataract; CATARACT; EXPRESSION;
D O I
10.1080/02713683.2023.2293457
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
PurposeAccumulated evidence has shown that microRNAs (miRNAs) are closely related to the pathogenesis and progression of senile cataracts. Here we investigate the effect of miR-29a-3p in cataractogenesis and determined the potential molecular mechanism involved.MethodsIn this study, we constructed a selenite cataract model in rats and obtained the miRNAs related to cataracts by whole transcriptome sequencing. To investigate the effect and mechanism of miR-29a-3p on cataracts, we performed several in vivo and in vitro experiments, including CCK8 assay, flow cytometry, luciferase reporter assay, Edu assay, and western blot analysis.ResultSequencing data showed downregulation of miR-29a-3p in rats with selenite cataracts. Down-regulation of miR-29a-3p could promote lens epithelial cells (SRA01/04) proliferation and inhibit cell apoptosis, and miR-29a-3p silence could inhibit the development of cataracts. Additionally, CAND1 was a direct target gene for miR-29a-3p.ConclusionThese data demonstrate that miR-29a-3p inhibits apoptosis of lens epithelial cells by regulating CAND1, which may be a potential target for senile cataracts.
引用
收藏
页码:391 / 400
页数:10
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