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本文引用的文献

1
Activation of oxidative stress-regulated Bcl-3 suppresses CTCF in corneal epithelial cells.氧化应激调节的 Bcl-3 激活抑制角膜上皮细胞中的 CTCF。
PLoS One. 2011;6(8):e23984. doi: 10.1371/journal.pone.0023984. Epub 2011 Aug 30.
2
Regulation of Pax6 by CTCF during induction of mouse ES cell differentiation.CTCF 在诱导小鼠胚胎干细胞分化过程中对 Pax6 的调控。
PLoS One. 2011;6(6):e20954. doi: 10.1371/journal.pone.0020954. Epub 2011 Jun 13.
3
Hyperosmotic stress-induced corneal epithelial cell death through activation of Polo-like kinase 3 and c-Jun.高渗应激通过激活 Polo 样激酶 3 和 c-Jun 诱导角膜上皮细胞死亡。
Invest Ophthalmol Vis Sci. 2011 May 16;52(6):3200-6. doi: 10.1167/iovs.10-6485.
4
Gene expression analysis in SV-40 immortalized human corneal epithelial cells cultured with an air-liquid interface.在气液界面培养的SV - 40永生化人角膜上皮细胞中的基因表达分析
Mol Vis. 2010 Oct 15;16:2109-20.
5
Control of actin filament treadmilling in cell motility.细胞运动中肌动蛋白丝的 treadmilling 控制。
Annu Rev Biophys. 2010;39:449-70. doi: 10.1146/annurev-biophys-051309-103849.
6
NF-kappaB subtypes regulate CCCTC binding factor affecting corneal epithelial cell fate.NF-κB 亚型调节 CCCTC 结合因子影响角膜上皮细胞命运。
J Biol Chem. 2010 Mar 26;285(13):9373-9382. doi: 10.1074/jbc.M109.094425. Epub 2010 Jan 28.
7
Effect of EGF-induced HDAC6 activation on corneal epithelial wound healing.表皮生长因子诱导的组蛋白去乙酰化酶 6 激活对角膜上皮伤口愈合的影响。
Invest Ophthalmol Vis Sci. 2010 Jun;51(6):2943-8. doi: 10.1167/iovs.09-4639. Epub 2010 Jan 20.
8
ERK1/2 mediate wounding- and G-protein-coupled receptor ligands-induced EGFR activation via regulating ADAM17 and HB-EGF shedding.细胞外信号调节激酶1/2通过调控金属蛋白酶17(ADAM17)和肝素结合表皮生长因子(HB-EGF)的脱落来介导伤口和G蛋白偶联受体配体诱导的表皮生长因子受体(EGFR)激活。
Invest Ophthalmol Vis Sci. 2009 Jan;50(1):132-9. doi: 10.1167/iovs.08-2246. Epub 2008 Jul 24.
9
Functional role of CCCTC binding factor (CTCF) in stress-induced apoptosis.CCCTC结合因子(CTCF)在应激诱导的细胞凋亡中的功能作用。
Exp Cell Res. 2007 Aug 15;313(14):3057-65. doi: 10.1016/j.yexcr.2007.05.018. Epub 2007 May 24.
10
Role of c-Fos/JunD in protecting stress-induced cell death.c-Fos/JunD在保护应激诱导的细胞死亡中的作用。
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CTCF 在表皮生长因子诱导的永生化人角膜上皮细胞迁移中的作用。

Role of CTCF in EGF-induced migration of immortalized human corneal epithelial cells.

机构信息

Department of Medicine, Jules Stein Eye Institute, David Geffen School of Medicine, University of California Los Angeles, CA 90502, USA.

出版信息

Invest Ophthalmol Vis Sci. 2012 Feb 23;53(2):946-51. doi: 10.1167/iovs.11-8747. Print 2012 Feb.

DOI:10.1167/iovs.11-8747
PMID:22247490
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3317431/
Abstract

PURPOSE

EGF-induced activation of the epigenetic CCCTC binding factor (CTCF) plays an important role in corneal epithelial cell proliferation by suppressing the Pax6 gene. The present study focused on further understanding the role of CTCF in mediating EGF-induced migration of immortalized human corneal epithelial cells.

METHODS

CTCF activities in human corneal epithelial cells immortalized by telomerase (HTCE cells) and SV-40 (HCE cells) transformation were suppressed and enhanced by CTCF mRNA knockdown and by overexpressing CTCF cDNA, respectively. EGF-induced cell migration was evaluated by linear scratch wound healing, a cell migration assay, and live cell motility GFP-tracking with a fluorescence microscope. Immunochemical analysis was performed for detecting focal adhesion changes in EGF-induced and CTCF activity-altered cells.

RESULTS

EGF-induced wound closure and cell migration rates of human corneal epithelial cells were significantly suppressed and enhanced by CTCF mRNA knockdown and by overexpression of CTCF, respectively. CTCF mRNA knockdown also markedly suppressed cell motility, determined by using a live-cell-tracking system in GFP-tag-expressed HTCE cells. Finally, alterations of EGF-stimulated focal adhesion were observed in CTCF knockdown HTCE cells by immunostaining of F-actin and vinculin in cytoskeleton reorganization.

CONCLUSIONS

CTCF, an epigenetic regulator and transcription factor, involves EGF-induced increases in cell motility and migration. CTCF plays an essential role in growth factor-regulated human corneal epithelial cell wound healing.

摘要

目的

表皮生长因子(EGF)诱导的表观遗传 CCCTC 结合因子(CTCF)的激活通过抑制 Pax6 基因在角膜上皮细胞增殖中发挥重要作用。本研究旨在进一步了解 CTCF 在介导永生化人角膜上皮细胞中 EGF 诱导的迁移中的作用。

方法

通过 CTCF mRNA 敲低和过表达 CTCF cDNA 分别抑制和增强端粒酶(HTCE 细胞)和 SV-40(HCE 细胞)转化的人角膜上皮细胞中的 CTCF 活性。通过线性划痕愈合、细胞迁移测定和荧光显微镜下 GFP 标记的活细胞运动追踪评估 EGF 诱导的细胞迁移。进行免疫化学分析以检测 EGF 诱导和 CTCF 活性改变细胞中的焦点粘连变化。

结果

EGF 诱导的人角膜上皮细胞的伤口闭合和细胞迁移率分别通过 CTCF mRNA 敲低和 CTCF 的过表达显著抑制和增强。CTCF mRNA 敲低也显著抑制了 GFP 标记的 HTCE 细胞中活细胞追踪系统测定的细胞运动。最后,通过细胞骨架重排中的 F-肌动蛋白和纽蛋白的免疫染色观察到 CTCF 敲低 HTCE 细胞中 EGF 刺激的焦点粘连的改变。

结论

作为一种表观遗传调节剂和转录因子,CTCF 参与 EGF 诱导的细胞迁移和迁移增加。CTCF 在生长因子调节的人角膜上皮细胞伤口愈合中起重要作用。