MIGRATION OF IEC-6 CELLS - A MODEL FOR MUCOSAL HEALING
MIGRATION OF IEC-6 CELLS - A MODEL FOR MUCOSAL HEALING
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DOI：
10.1152/ajpgi.1992.263.3.g426
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发表时间：
1992-09-01
影响因子：
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通讯作者：
JOHNSON, LR
中科院分区：
文献类型：
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作者：
MCCORMACK, SA;VIAR, MJ;JOHNSON, LR
细胞迁移是胃肠道粘膜糜烂早期恢复的主要力量。尽管细胞迁移对愈合的重要性，但没有尝试在培养中研究这一过程的报道。我们试图标准化小肠上皮隐窝细胞系IEC-6的迁移条件，并在一些已知的体内实验条件下测试其迁移反应。结果表明：1)迁移不依赖于DNA合成；2) DNA合成不集中在创口边缘；3)抑制肌动蛋白聚合完全停止迁移。此外，细胞外基质的存在使迁移最大化。不同作用方式的蛋白质抑制剂对细胞迁移的抑制程度不同，并不总是与其对蛋白质合成的抑制程度相称。细胞表面蛋白聚糖很重要；透明质酸有作用，但损伤细胞分泌一种刺激迁移的物质是不确定的。值得注意的是，抑制鸟氨酸脱羧酶和多胺合成的α -二氟甲基鸟氨酸（DFMO）几乎完全阻止了细胞迁移。由于DFMO在体内也能阻止粘膜糜烂的愈合，我们认为该模型可以在考虑到其空间局限性的情况下，用于研究参与粘膜糜烂早期修复的细胞迁移过程。
Cell migration is the principal force behind the early restitution of erosions of the mucosa of the gastrointestinal tract. Despite the importance of cell migration to healing, no attempts to study the process in culture have been reported. We have attempted to standardize conditions for migration and test the migration responses of the small intestinal epithelial crypt cell line IEC-6 in some experimental situations already well known in vivo. We found good correspondence between in culture and in vivo on the following points: 1) migration was independent of DNA synthesis; 2) DNA synthesis was not concentrated at the wound edge; and 3) inhibition of actin polymerization stopped migration altogether. In addition, the presence of an extracellular matrix maximized migration. Protein inhibitors with different modes of action inhibited cell migration to different degrees, not always commensurate with their inhibition of protein synthesis. Cell surface proteoglycans were important; hyaluronic acid had an effect, but the secretion of a migration-stimulating substance by wounded cells was equivocal. Significantly, alpha-difluoromethylornithine (DFMO), which inhibits ornithine decarboxylase and polyamine synthesis, almost totally prevented cell migration. Because DFMO also prevents healing of mucosal erosions in vivo, we believe that this model can be used, keeping in mind its spatial limitations, to study the process of cell migration involved in the early restitution of mucosal erosions.