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Antagonistic regulation of cell migration by epidermal growth factor and glucocorticoid.

表皮生长因子和糖皮质激素对细胞迁移的拮抗调节。

基本信息

批准号：
09672265
负责人：
ITO Fumiaki
金额：
$ 2.05万
依托单位：
SETSUNAN UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09672265/
关键词：
Epidermal growth factor Glucocorticoid Integrin Cell migration Extracellular matrix Collagen Cell adhesion 接着斑

项目摘要

Cell migration is a critical event in morphogenesis, tissue repair inflammatory reactions, and interactions in the immune system. A variety of growth factors such as epidermal growth factor (EGF) have been known to stimulate cell migration. In fact, we found that EGF stimulated cell migration of TMK-l, a cell line derived from a human gastric carcinoma. In this study, we have reported that the EGF-induced cell migration was inhibited if the cells were pretreated with dexamethasone, a synthetic glucocorticoid. Since interaction of cells with a variety of extracellular matrices such as collagen, fibronectin, and laminin is thought to be crucial for cell migration, we studied the effect of glucocorticoid and EGF on cell adhesion of TMK-1 to extracellular matrices. Dexamethasone increased cell adhesion to collagen typelV and laminin, but not to poly-L-lysine and fibronectin. In contrast, EGF did not affect cell adhesion to these extracellular matrices whether dexamethasone was present or n … More ot.Cell-extracellular matrix interactions are mediated by a family of integriris, each of which is a cell-surface protein consisting of an alpha subunit noncovalently associated with a beta subunit. We then examined the expression level of a variety of alpha and beta subunits in TMK-1 cells which had been pretreated with dexamethasone or EGF.Dexamethasone enhanced the protein levels of both alpha 1 and beta 1 integrin subunits, and that of the alpha1beta 1 heterodimer. Further, flow cytometric analysis revealed that dexamethasone increased the expression of alpha 1and beta 1 subunits at the cell surface, whereas EGF increased expression of alpha 2 and beta 1 subunits at the cell surface. Antibodies against alpha 1 and beta 1 integrin subunits inhibited the increased cell adhesion seen in the presence of dexamethasone. These results suggest that glucocorticoid increased cell adhesion to the extracellular matrix via alpha 1beta1 integrin, and thereby antagonized EGF-induced cell migration. Less

细胞迁移是形态发生、组织修复炎症反应和免疫系统相互作用中的关键事件。已知多种生长因子如表皮生长因子（EGF）刺激细胞迁移。事实上，我们发现EGF刺激TMK-1细胞迁移，TMK-1是一种来源于人胃癌的细胞系。在这项研究中，我们已经报道，抑制EGF诱导的细胞迁移，如果细胞用地塞米松，合成糖皮质激素预处理。由于细胞与各种细胞外基质如胶原蛋白、纤连蛋白和层粘连蛋白的相互作用被认为是细胞迁移的关键，我们研究了糖皮质激素和EGF对TMK-1细胞粘附到细胞外基质的影响。地塞米松增加细胞对1V型胶原和层粘连蛋白的粘附，但不增加细胞对多聚赖氨酸和纤连蛋白的粘附。相反，EGF不影响细胞与这些细胞外基质的粘附，无论是否存在地塞米松。 ...更多信息细胞-细胞外基质相互作用由整联蛋白家族介导，每一个整联蛋白家族都是由与β亚基非共价结合的α亚基组成的细胞表面蛋白。然后我们检测了用地塞米松或EGF预处理的TMK-1细胞中各种α和β亚基的表达水平，地塞米松增强了α 1和β 1整合素亚基以及α 1 β 1异二聚体的蛋白水平。此外，流式细胞仪分析显示，地塞米松增加α 1和β 1亚基在细胞表面的表达，而EGF增加α 2和β 1亚基在细胞表面的表达。针对α 1和β 1整联蛋白亚基的抗体抑制了在地塞米松存在下观察到的增加的细胞粘附。这些结果表明，糖皮质激素增加细胞粘附细胞外基质通过α 1 β 1整合素，从而拮抗EGF诱导的细胞迁移。少