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由E-钙黏蛋白(卵清黏蛋白)介导的细胞间接触限制了L细胞的侵袭行为。

Cell-cell contacts mediated by E-cadherin (uvomorulin) restrict invasive behavior of L-cells.

作者信息

Chen W C, Obrink B

机构信息

Department of Medical Cell Biology, Medical Nobel Institute, Karolinska Institute, Stockholm, Sweden.

出版信息

J Cell Biol. 1991 Jul;114(2):319-27. doi: 10.1083/jcb.114.2.319.

DOI:10.1083/jcb.114.2.319
PMID:1649199
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2289070/
Abstract

L-cells were cotransfected with plasmids coding for mouse E-cadherin (uvomorulin) and the neophosphotransferase gene, and stable transfectants expressing E-cadherin at the cell surface were selected and cloned. Control transfection was done with the neophosphotransferase gene alone. The invasive migration of transfected and untransfected L-cells into three-dimensional collagen gels was then analyzed. L-cells not expressing E-cadherin migrated efficiently into the gels, whereas invasion of the E-cadherin-expressing L-cells was restricted in a cell density dependent manner. At sparse density, when the cells exhibited little cell-cell contacts, no difference was observed between the level of invasion of the cadherin-expressing cells and the control cells. However, with increasing cell density, decreasing amounts of the cadherin-expressing cells but increasing amounts of the control cells migrated into the gels. At confluent density hardly any cadherin-expressing cells were able to migrate into the gels. The inhibition of the invasion of the cadherin-expressing cells could be reverted if confluent cells were cultured in the presence of monoclonal antibodies against E-cadherin. Since the expression of E-cadherin did not influence the invasive mobility of single cells, these results indicate that E-cadherin-mediated cell-cell contacts inhibited invasive cellular migration. Time-lapse videoscopy and studies of cell migration from a monolayer into a cell-free area demonstrated that the restricted invasion could be explained by contact inhibition of cell movement of the cadherin-expressing cells.

摘要

将L细胞与编码小鼠E-钙黏蛋白(桥粒芯蛋白)的质粒和新磷酸转移酶基因共转染,然后选择并克隆在细胞表面表达E-钙黏蛋白的稳定转染子。单独用新磷酸转移酶基因进行对照转染。接着分析转染和未转染的L细胞向三维胶原凝胶中的侵袭性迁移。不表达E-钙黏蛋白的L细胞能有效地迁移到凝胶中,而表达E-钙黏蛋白的L细胞的侵袭则以细胞密度依赖性方式受到限制。在低密度时,当细胞间几乎没有细胞间接触时,表达钙黏蛋白的细胞和对照细胞的侵袭水平没有差异。然而,随着细胞密度增加,迁移到凝胶中的表达钙黏蛋白的细胞数量减少,而对照细胞数量增加。在汇合密度时,几乎没有表达钙黏蛋白的细胞能够迁移到凝胶中。如果汇合细胞在抗E-钙黏蛋白单克隆抗体存在下培养,表达钙黏蛋白的细胞的侵袭抑制可被逆转。由于E-钙黏蛋白的表达不影响单个细胞的侵袭迁移能力,这些结果表明E-钙黏蛋白介导的细胞间接触抑制了细胞的侵袭性迁移。延时视频显微镜检查以及对细胞从单层迁移到无细胞区域的研究表明,表达钙黏蛋白的细胞的运动接触抑制可以解释侵袭受限的原因。

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