miR-30a reverses TGF-β2-induced migration and EMT in posterior capsular opacification by targeting Smad2

被引：25

作者：

Li, Hua ^{[1
]}

Song, Hui ^{[1
]}

Yuan, Xiaoyong ^{[1
]}

Li, Jun ^{[1
]}

Tang, Hua ^{[2
,3
]}

机构：

[1] Tianjin Med Univ, Tianjin Eye Hosp, Clin Coll Ophthalmol, Tianjin, Peoples R China

[2] Tianjin Med Univ, Tianjin Life Sci Res Ctr, Tianjin, Peoples R China

[3] Tianjin Med Univ, Dept Pathogen Biol, Tianjin, Peoples R China

来源：

MOLECULAR BIOLOGY REPORTS | 2019年 / 46卷 / 04期

基金：

中国国家自然科学基金; 中国博士后科学基金;

关键词：

miR-30a; TGF-beta; 2; Smad2; Posterior capsular opacification; TO-MESENCHYMAL TRANSITION; LENS; PROLIFERATION; RECEPTOR;

D O I：

10.1007/s11033-019-04833-4

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Posterior capsular opacification (PCO) leads to secondary vision loss following cataract surgery. TGF-beta 2 and miRNA play important roles in PCO. The aim of this study was to investigate the reciprocal crosstalk between miR-30a and TGF-beta 2/Smad2 during PCO progression. The expressions of and relationship between miR-30a and Smad2 were detected by RT-qPCR. Migration and epithelial-mesenchymal transition (EMT) were used to evaluate the functions of miR-30a and TGF-beta 2/Smad2. We found that miR-30a was downregulated by TGF-beta 2 and that it suppressed migration and EMT induced by TGF-beta 2. Moreover, we identified Smad2 as a direct target of miR-30a, suggesting that miR-30a may function partly through regulating Smad2. Altogether, we verified the function of and crosstalk between miR-30a and TGF-beta 2. We also provide evidence that miR-30a may serve as a potential candidate for PCO treatment.

引用

页码：3899 / 3907

页数：9

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