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转化生长因子β1(TGF-β1)刺激整合素连接激酶(ILK)通过核因子κB(NF-κB)调节人晶状体上皮细胞的迁移和上皮-间充质转化(EMT)。

Transforming Growth Factor β1 (TGF-β1)-Stimulated Integrin-Linked Kinase (ILK) Regulates Migration and Epithelial-Mesenchymal Transition (EMT) of Human Lens Epithelial Cells via Nuclear Factor κB (NF-κB).

机构信息

Tianjin Eye Hospital, Clinic College of Ophthalmology, Tianjin Medical University, Tianjin, China (mainland).

出版信息

Med Sci Monit. 2018 Oct 17;24:7424-7430. doi: 10.12659/MSM.910601.

DOI:10.12659/MSM.910601
PMID:30332398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6201705/
Abstract

BACKGROUND In view of the high incidence of posterior capsule opacification (PCO) and the effects of TGF-β signaling on the epithelial-mesenchymal transition (EMT) of human lens epithelial cells (LECs), our study aimed to explore the mechanism of the function of TGF-β signaling in LECs EMT. MATERIAL AND METHODS Human lens epithelial cells (HLEC-h3) were treated with TGF-β, ILK siRNA, ILK inhibitor, and NF-κB inhibitor to study the effects of TGF-β, ILK, and NF-κB on cell migration and EMT. Cell migration assay was used to measure cell migration ability. Western blot was performed to detect the expression of ILK, E-cadherin, and a-SMA at the protein level. QRT-PCR was used to detect the expression of ILK at the mRNA level. RESULTS Compared with control cells, TGF-β treatment increased the expression level of ILK HLEC-h3, promoted migration of HLEC-h3 cells, increased the expression level of E-cadherin protein, and decreased the expression level of a-SMA protein. However, treatment with ILK siRNA, ILK inhibitor, and NF-κB inhibitor reversed the effects of TGF-β on HLEC-h3 cells. CONCLUSIONS TGF-β-stimulated ILK regulates the migration and EMT of human LECs via NF-κB.

摘要

背景

鉴于后囊膜混浊(PCO)的高发病率,以及 TGF-β 信号对人晶状体上皮细胞(LEC)上皮间质转化(EMT)的影响,我们旨在探讨 TGF-β 信号在 LECs EMT 中的功能机制。

材料和方法

用 TGF-β、ILK siRNA、ILK 抑制剂和 NF-κB 抑制剂处理人晶状体上皮细胞(HLEC-h3),以研究 TGF-β、ILK 和 NF-κB 对细胞迁移和 EMT 的影响。细胞迁移实验用于测量细胞迁移能力。Western blot 用于检测 ILK、E-钙黏蛋白和 a-SMA 蛋白的表达水平。QRT-PCR 用于检测 ILK 的 mRNA 表达水平。

结果

与对照组细胞相比,TGF-β 处理增加了 HLEC-h3 中 ILK 的表达水平,促进了 HLEC-h3 细胞的迁移,增加了 E-钙黏蛋白蛋白的表达水平,降低了 a-SMA 蛋白的表达水平。然而,用 ILK siRNA、ILK 抑制剂和 NF-κB 抑制剂处理后,TGF-β 对 HLEC-h3 细胞的作用被逆转。

结论

TGF-β 刺激的 ILK 通过 NF-κB 调节人 LECs 的迁移和 EMT。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e76/6201705/52019d9da911/medscimonit-24-7424-g005.jpg
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