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转化生长因子-β1在人HERS/ERM细胞上皮-间质转化过程中对粒细胞-巨噬细胞集落刺激因子的上调作用

Upregulation of GM-CSF by TGF-β1 in epithelial mesenchymal transition of human HERS/ERM cells.

作者信息

Lee Joo-Hee, Nam Hyun, Um Soyoun, Lee Juhwan, Lee Gene, Seo Byoung Moo

机构信息

Biotooth Engineering Lab, Department of Oral and Maxillofacial Surgery, School of Dentistry, Craniomaxillofacial Life Science, Dental Research Institute, Seoul National University, Seoul, South Korea.

出版信息

In Vitro Cell Dev Biol Anim. 2014;50(5):399-405. doi: 10.1007/s11626-013-9712-3. Epub 2013 Nov 21.

DOI:10.1007/s11626-013-9712-3
PMID:24258001
Abstract

Hertwig's epithelial root sheath/epithelial rests of Malassez (HERS/ERM) have been suggested to play an important role in tooth root formation, particularly in periodontal development. Epithelial mesenchymal transition (EMT) has been suggested to contribute to root development in tooth. However, the mechanism of interaction between HERS/ERM cells and dental mesenchymal cells has not been fully understood. In this study, we investigated the effect of exogenous transforming growth factor beta 1 (TGF-β1) in human HERS/ERM cells in order to verify the role of granulocyte macrophage colony-stimulating factor (GM-CSF) in EMT process. Antibody array was used to screen secretion factors by exogenous TGF-β1. Secretion of GM-CSF was increased by exogenous TGF-β1. Expression levels of EMT markers, vimentin, ZEB1 (zinc finger E-box binding homeobox 1), and E-cadherin, were confirmed using reverse transcription polymerase chain reaction and immunocytochemistry. Treatment with GM-CSF increased the expression of vimentin and ZEB1, similar to TGF-β1 treatment, and decreased the expression of E-cadherin. Our results suggest that GM-CSF could induce EMT in human HERS/ERM cells.

摘要

赫特维希上皮根鞘/马拉瑟上皮剩余(HERS/ERM)被认为在牙根形成中发挥重要作用,尤其是在牙周发育方面。上皮-间充质转化(EMT)被认为有助于牙齿的牙根发育。然而,HERS/ERM细胞与牙间充质细胞之间的相互作用机制尚未完全阐明。在本研究中,我们研究了外源性转化生长因子β1(TGF-β1)对人HERS/ERM细胞的影响,以验证粒细胞巨噬细胞集落刺激因子(GM-CSF)在EMT过程中的作用。使用抗体芯片筛选外源性TGF-β1诱导的分泌因子。外源性TGF-β1可增加GM-CSF的分泌。利用逆转录聚合酶链反应和免疫细胞化学技术检测EMT标志物波形蛋白、锌指E盒结合同源框1(ZEB1)和E-钙黏蛋白的表达水平。与TGF-β1处理相似,GM-CSF处理可增加波形蛋白和ZEB1的表达,并降低E-钙黏蛋白的表达。我们的结果表明,GM-CSF可诱导人HERS/ERM细胞发生EMT。

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