STUDIES ON MECHANISMS OF CELL-MIGRATION .1. MECHANISM OF FIBRONECTIN-MEDIATED CELL-MIGRATION - DEPENDENCE OR INDEPENDENCE OF CELL-MIGRATION SUSCEPTIBILITY ON RGDS-DIRECTED RECEPTOR (INTEGRIN)
STUDIES ON MECHANISMS OF CELL-MIGRATION .1. MECHANISM OF FIBRONECTIN-MEDIATED CELL-MIGRATION - DEPENDENCE OR INDEPENDENCE OF CELL-MIGRATION SUSCEPTIBILITY ON RGDS-DIRECTED RECEPTOR (INTEGRIN)
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DOI：
10.1016/0014-4827(89)90423-0
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发表时间：
1989-07-01
影响因子：
3.7
通讯作者：
HAKOMORI, SI
中科院分区：
文献类型：
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作者：
STRAUS, AH;CARTER, WG;HAKOMORI, SI
使用10个细胞系研究了纤连蛋白（FN）包被的基质上的细胞迁移，其中只有2个显示出明显的细胞迁移增强，1个显示出细胞迁移的边缘增强。其他 7 个细胞系的迁移不受 FN 包被基质的影响，尽管它们都表现出 FN 依赖性细胞粘附。在包括细胞粘附和 Hep-2 结构域的片段中发现了 FN 的迁移增强活性，但在其他结构域（Hep-1/Feb-1、Gel.Fib-2）中没有发现。来自血浆、成纤维细胞或转化细胞的 FN 的迁移增强作用没有差异。 FN依赖性细胞迁移被针对C端半区（包括细胞结合结构域）的多克隆抗体抑制，但不被针对其他五个结构域的抗体抑制。由于这些结果表明 FN 介导的细胞迁移可以通过 FN 及其受体的细胞粘附持续时间来控制，因此研究的重点是针对 FN 和胶原蛋白受体的抗体的作用，以及这些受体识别的四肽序列的作用。结果发现，(i) FN 包被表面上的细胞迁移被抗 FN 受体抗体 P1F8 特异性抑制，但不被抗胶原受体抗体 P1H5 抑制：(ii) 迁移被 Arg-Gly-Asp-Ser 强烈抑制，但不被其他寡肽序列强烈抑制。然而，大多数对 FN 依赖性细胞迁移不敏感的细胞系的特征是具有 FN 受体并能够粘附在 FN 包被的基质上。基于这些发现，得出结论：FN依赖性细胞迁移与FN依赖性细胞粘附具有相同的识别机制，但大多数不表现出FN依赖性迁移的细胞系仍然表现出FN依赖性细胞粘附并表达FN受体（整合素）；即细胞迁移和粘附涉及相同的受体和相同的 FN 位点，但迁移是由尚未确定的细胞因子控制的，这些细胞因子决定细胞对 FN 受体（整合素）单元的动态功能的敏感性。
Cell migration on fibronectin (FN)-coated substrata was studed using 10 cell lins, of which only 2 showed clear enhancement and 1 showed marginal enhancement of cell migration. The migration of the other 7 cell lines was not affected on FN-coated substrata, although they all showed FN-dependent cell adhesion. The migration-enhancing activity of FN was found in the fragment including the cell-adhesion and Hep-2 domains, but not other domains (Hep-1/Feb-1, Gel. Fib-2). No difference in the migration-enhancing effect was seen among FNs from plasma, fibroblasts, or transformed cells. FN-dependent cell migration was inhibited by polyclonal antibodies directed to the C-terminal half region including the cell binding domain, but not by antibodies directed to five other domains. Since these results indicated that FN-mediated cell migration could be controlled by the cell-adhesion duration of FN and its receptor, studies were then focused on the effect of antibodies directed to receptors for FN and collagen, and on the effect of tetrapeptide sequences recognized by these receptors. It was found that (i) cell migration on FN-coated surfaces was specifically inhibited by anti-FN receptor antibody P1F8 but not by anticollagen receptor antibody P1H5: (ii) the migration was strongly inhibited by Arg-Gly-Asp-Ser but not by other oligopeptide sequences. However, the majority of those cell lines not susceptible to FN-dependent cell migration were characterized by having FN receptors and the ability to adhere on FN-coated matrix. Based on these findings, it was concluded that FN-dependent cell migration shares the same recognition mechanism as FN-dependent cell adhesion, but that the majority of cell lines not exhibiting FN-dependent migration still shown FN-dependent cell adhesion and express the FN receptor (integrin); i.e. cell migration and adhesion involve the same receptor and the same FN loci, but migration is controlled by still-unidentified cellular factors which determine the susceptibity of the cell to the dynamic function of the FN receptor (integrin) unit.