环状 RNA 0080940 通过调控 miR-139-5p/CTGF 通路促进人眼Tenon 囊成纤维细胞的增殖、迁移和细胞外基质沉积。
Circ_0080940 Regulates miR-139-5p/CTGF Pathway to Promote the Proliferation, Migration, Extracellular Matrix Deposition of Human Tenon's Capsule Fibroblasts.
机构信息
Department of Ophthalmology, the Affiliated Hospital of Southwest Medical University, Luzhou, China.
出版信息
Curr Eye Res. 2023 Jan;48(1):34-43. doi: 10.1080/02713683.2022.2138449. Epub 2022 Nov 4.
PURPOSE
Circular RNA (circRNA) has been identified as an important regulator for glaucoma progression. Our study aims to reveal the circ_0080940 roles in glaucoma progression.
METHODS
Transforming growth factor β1 (TGF-β1) was used to treat human Tenon's capsule fibroblasts (HTFs) to mimic glaucoma cell models. Cell function was determined by cell counting kit 8 assay, EdU assay and wound healing assay. Protein levels were determined by western blot analysis. Quantitative real-time PCR was used to measure RNA expression. Dual-luciferase reporter assay was performed to evaluate RNA interaction.
RESULTS
Our data confirmed that TGF-β1 induced HTFs proliferation, migration and extracellular matrix (ECM) deposition. Circ_0080940 was highly expressed in glaucoma patients, and its knockdown inhibited TGF-β1-induced proliferation, migration and ECM deposition in HTFs. Circ_0080940 sponged miR-139-5p, and anti-miR-139-5p revoked the effect of si-circ_0080940 on the biological functions of TGF-β1-induced HTFs. CTGF was targeted by miR-139-5p, and overexpressed CTGF overturned the inhibition effect of miR-139-5p on the biological functions of TGF-β1-induced HTFs. Furthermore, CTGF expression could be positively regulated by circ_0080940.
CONCLUSION
To sum up, we confirmed that circ_0080940 contributed to glaucoma progression by miR-139-5p/CTGF axis.
目的
环状 RNA（circRNA）已被确定为青光眼进展的重要调节因子。本研究旨在揭示 circ_0080940 在青光眼进展中的作用。
方法
用转化生长因子β1（TGF-β1）处理人Tenon's 囊成纤维细胞（HTFs），模拟青光眼细胞模型。通过细胞计数试剂盒 8 检测、EdU 检测和划痕愈合实验检测细胞功能。通过 Western blot 分析检测蛋白水平。采用定量实时 PCR 检测 RNA 表达。采用双荧光素酶报告基因检测评估 RNA 相互作用。
结果
我们的数据证实，TGF-β1 诱导 HTFs 增殖、迁移和细胞外基质（ECM）沉积。circ_0080940 在青光眼患者中高表达，其敲低抑制 TGF-β1 诱导的 HTFs 增殖、迁移和 ECM 沉积。circ_0080940 海绵吸附 miR-139-5p，抗 miR-139-5p 逆转了 si-circ_0080940 对 TGF-β1 诱导的 HTFs 生物学功能的影响。CTGF 是 miR-139-5p 的靶基因，过表达 CTGF 推翻了 miR-139-5p 对 TGF-β1 诱导的 HTFs 生物学功能的抑制作用。此外，CTGF 的表达可被 circ_0080940 正向调节。
结论
综上所述，我们证实 circ_0080940 通过 miR-139-5p/CTGF 轴促进青光眼进展。
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