Albers T M, Lomakina I, Moore R P
Department of Pathology, Tufts University, School of Medicine and Veterinary Medicine, Boston, Massachusetts, USA.
Lab Invest. 1995 Jul;73(1):139-48.
Maintenance of enterocyte polarity is crucial to normal intestinal function. Tight junctions and cell-matrix interactions play a role in maintaining polarized cell membrane domains. In many intestinal epithelial wounds, normal cell-cell associations mediated by tight junctions are lost. The goal of this study was to examine the fate of an apically restricted fucosylated glycoconjugate (FGC) and basolaterally restricted Na/K-ATPase in a model of intestinal epithelial repair. Comparisons are made to isolated enterocytes in which cell-matrix interactions are disrupted as well.
We present a novel physiologically relevant model of intestinal epithelial injury and restitution that was used to examine the fate of two polarized membrane components by fluorescent and ultrastructural techniques. In addition, we used mechanical vibration to isolate enterocytes as individual and short sheets of cells from the intestinal basement membrane and evaluated the fate of these restricted membrane components using immuno- and lectin histochemistry.
Na/K-ATPase maintained its basolateral membrane location in restituting epithelial but relocated to a nonbasolateral position in the majority of isolated enterocytes. The FGC maintained its apical restriction in isolated enterocytes and in epithelial cells migrating across denuded basement membrane. An additional and important observation noted in this study was a drastic alteration in shape of migrating epithelial cells characterized by diminution and loss of microvilli as the cells migrated across the injury.
We conclude from our results that maintenance of Na/K-ATPase to a basolateral membrane position is influenced by cell-matrix interactions. In contrast, restriction of FGC to the apical membrane of enterocytes is dependent on the presence of microvilli and is not related to either cell-cell or cell-matrix interactions. Additionally, we suggest a new model of intestinal repair in which microvilli are disassembled. We speculate that membrane from disassembled microvilli, as well as lateral cell membrane, are used at the leading edge of the migrating cell.
肠上皮细胞极性的维持对正常肠道功能至关重要。紧密连接和细胞与基质的相互作用在维持极化细胞膜结构域中发挥作用。在许多肠道上皮伤口中，由紧密连接介导的正常细胞间联系会丧失。本研究的目的是在肠道上皮修复模型中研究顶端受限的岩藻糖基化糖缀合物（FGC）和基底外侧受限的钠钾ATP酶的命运。同时也对细胞与基质相互作用被破坏的分离肠上皮细胞进行了比较。
我们提出了一种新的与生理相关的肠道上皮损伤和修复模型，通过荧光和超微结构技术来研究两种极化膜成分的命运。此外，我们使用机械振动从肠道基底膜分离出单个和短细胞片的肠上皮细胞，并使用免疫组织化学和凝集素组织化学评估这些受限膜成分的命运。
钠钾ATP酶在修复的上皮细胞中维持其基底外侧膜位置，但在大多数分离的肠上皮细胞中重新定位到非基底外侧位置。FGC在分离的肠上皮细胞和跨裸露基底膜迁移的上皮细胞中维持其顶端限制。本研究中另一个重要观察结果是迁移的上皮细胞形状发生剧烈改变，其特征是细胞在损伤处迁移时微绒毛减少和丧失。
我们从结果中得出结论，钠钾ATP酶维持在基底外侧膜位置受细胞与基质相互作用的影响。相比之下，FGC限制在肠上皮细胞顶端膜取决于微绒毛的存在，与细胞间或细胞与基质相互作用均无关。此外，我们提出了一种微绒毛解体的肠道修复新模型。我们推测，解体微绒毛的膜以及细胞侧面的膜在迁移细胞的前沿被利用。
