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miR-30a 通过靶向 Smad2 逆转 TGF-β2 诱导的后囊膜混浊中的迁移和 EMT。

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

机构信息

Clinical College of Ophthalmology, Tianjin Medical University, Tianjin Eye Hospital, Tianjin, China.

Tianjin Life Science Research Center and Department of Pathogen Biology, Tianjin Medical University, Tianjin, China.

出版信息

Mol Biol Rep. 2019 Aug;46(4):3899-3907. doi: 10.1007/s11033-019-04833-4. Epub 2019 May 2.

DOI:10.1007/s11033-019-04833-4
PMID:31049834
Abstract

Posterior capsular opacification (PCO) leads to secondary vision loss following cataract surgery. TGF-β2 and miRNA play important roles in PCO. The aim of this study was to investigate the reciprocal crosstalk between miR-30a and TGF-β2/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-β2/Smad2. We found that miR-30a was downregulated by TGF-β2 and that it suppressed migration and EMT induced by TGF-β2. 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-β2. We also provide evidence that miR-30a may serve as a potential candidate for PCO treatment.

摘要

后囊膜混浊(PCO)导致白内障手术后继发性视力丧失。TGF-β2 和 miRNA 在 PCO 中发挥重要作用。本研究旨在探讨 miR-30a 和 TGF-β2/Smad2 在 PCO 进展过程中的相互串扰。通过 RT-qPCR 检测 miR-30a 和 Smad2 的表达及相关性。迁移和上皮间质转化(EMT)用于评估 miR-30a 和 TGF-β2/Smad2 的功能。我们发现 TGF-β2 下调了 miR-30a,并且它抑制了 TGF-β2 诱导的迁移和 EMT。此外,我们鉴定出 Smad2 是 miR-30a 的直接靶标,表明 miR-30a 可能部分通过调节 Smad2 发挥作用。总的来说,我们验证了 miR-30a 和 TGF-β2 之间的功能和串扰。我们还提供了证据表明,miR-30a 可能是 PCO 治疗的潜在候选药物。

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