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长链非编码 RNA 通过维持晶状体上皮细胞表型来预防晶状体纤维化。

Long Non-Coding RNA Prevents Lens Fibrosis through Maintaining Lens Epithelial Cell Phenotypes.

机构信息

State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou 510060, China.

出版信息

Cells. 2022 Aug 17;11(16):2559. doi: 10.3390/cells11162559.

DOI:10.3390/cells11162559
PMID:36010635
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9406623/
Abstract

The integrity of lens epithelial cells (LECs) lays the foundation for lens function and transparency. By contrast, epithelial-mesenchymal transition (EMT) of LECs leads to lens fibrosis, such as anterior subcapsular cataracts (ASC) and fibrotic forms of posterior capsule opacification (PCO). However, the underlying mechanisms remain unclear. Here, we aimed to explore the role of long non-coding RNA (lncRNA) in regulating TGF-β2-induced EMT during lens fibrosis, revealing a novel lncRNA-based regulatory mechanism. In this work, we identified that lncRNA H19 was highly expressed in LECs, but downregulated by exposure to TGF-β2. In both human lens epithelial explants and SRA01/04 cells, knockdown of aggravated TGF-β2-induced EMT, while overexpressing partially reversed EMT and restored lens epithelial phenotypes. Semi-in vivo whole lens culture and knockout mice demonstrated the indispensable role of in sustaining lens clarity through maintaining LEC features. Bioinformatic analyses further implied a potential -centered regulatory mechanism via Smad-dependent pathways, confirmed by in vitro experiments. In conclusion, we uncovered a novel role of in inhibiting TGF-β2-induced EMT of the lens by suppressing Smad-dependent signaling, providing potential therapeutic targets for treating lens fibrosis.

摘要

晶状体上皮细胞 (LEC) 的完整性为晶状体功能和透明性奠定了基础。相比之下，LEC 的上皮-间充质转化 (EMT) 会导致晶状体纤维化，如前囊下白内障 (ASC) 和后囊混浊 (PCO) 的纤维性形式。然而，其潜在机制尚不清楚。在这里，我们旨在探讨长链非编码 RNA (lncRNA) 在调节 TGF-β2 诱导的晶状体纤维化过程中的 EMT 中的作用，揭示了一种新的基于 lncRNA 的调控机制。在这项工作中，我们发现 lncRNA H19 在 LEC 中高度表达，但暴露于 TGF-β2 会下调其表达。在人晶状体上皮外植体和 SRA01/04 细胞中，敲低 加剧了 TGF-β2 诱导的 EMT，而过表达 部分逆转了 EMT 并恢复了晶状体上皮表型。半体内全晶状体培养和 敲除小鼠证明了 通过维持 LEC 特征在维持晶状体清晰度方面的不可或缺的作用。生物信息学分析进一步暗示了一种通过 Smad 依赖性途径的 - 中心调控机制，通过体外实验得到了证实。总之，我们揭示了 通过抑制 Smad 依赖性信号抑制 TGF-β2 诱导的晶状体 EMT 的新作用，为治疗晶状体纤维化提供了潜在的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/2fa522ca2d82/cells-11-02559-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/f879fa383655/cells-11-02559-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/a1bf938886c9/cells-11-02559-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/5674bd5c8de5/cells-11-02559-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/318fe456b400/cells-11-02559-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/bf25fc3175af/cells-11-02559-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/2fa522ca2d82/cells-11-02559-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/f879fa383655/cells-11-02559-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/4c17ba39a274/cells-11-02559-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/be6731575870/cells-11-02559-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/a1bf938886c9/cells-11-02559-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/5674bd5c8de5/cells-11-02559-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/31d7/9406623/318fe456b400/cells-11-02559-g007.jpg
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