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上皮细胞管状发生的形态发生机制:在分散因子/肝细胞生长因子诱导的管状发生过程中,MDCK细胞极性会短暂重排,且细胞间接触未丧失。

Morphogenetic mechanisms of epithelial tubulogenesis: MDCK cell polarity is transiently rearranged without loss of cell-cell contact during scatter factor/hepatocyte growth factor-induced tubulogenesis.

作者信息

Pollack A L, Runyan R B, Mostov K E

机构信息

Department of Anatomy, Department of Biochemistry and Biophysics, and Cardiovascular Research Institute, University of California at San Francisco, San Francisco, California, 94143,

出版信息

Dev Biol. 1998 Dec 1;204(1):64-79. doi: 10.1006/dbio.1998.9091.

Abstract

Many organ systems are composed of networks of epithelial tubes. Recently, molecules that induce development of epithelial tubules and regulate sites of branching have been identified. However, little is known about the mechanisms regulating cell rearrangements that are necessary for tubule formation. In this study we have used a scatter factor/hepatocyte growth factor-induced model system of MDCK epithelial cell tubulogenesis to analyze the mechanisms of cell rearrangement during tubule development. We examined the dynamics of cell polarity and cell-cell junctions during tubule formation and present evidence for a multistep model of tubulogenesis in which cells rearrange without loss of cell-cell contacts and tubule lumens form de novo. A three-dimensional analysis of markers for apical and basolateral membrane subdomains shows that epithelial cell polarity is transiently lost and subsequently regained during tubulogenesis. Furthermore, components of cell-cell junctional complexes undergo profound rearrangements: E-cadherin is randomly distributed around the cell surface, desmoplakins I/II accumulate intracellularly, and the tight junction protein ZO-1 remains localized at sites of cell-cell contact. This suggests that differential regulation of cell-cell junctions is important for the formation of tubules. Therefore, during tubulogenesis, cell-cell adhesive contacts are differentially regulated while the polarity and specialization of plasma membrane subdomains reorganize, enabling cells to remain in contact as they rearrange into new structures.

摘要

许多器官系统由上皮管网络组成。最近,已鉴定出诱导上皮小管发育并调节分支位点的分子。然而,对于调节小管形成所必需的细胞重排机制知之甚少。在本研究中,我们使用了散射因子/肝细胞生长因子诱导的MDCK上皮细胞小管形成模型系统,来分析小管发育过程中的细胞重排机制。我们研究了小管形成过程中细胞极性和细胞间连接的动态变化,并提出了一个多步骤的小管形成模型,其中细胞在不丧失细胞间接触的情况下重排,并且小管腔从头形成。对顶膜和基底外侧膜亚结构域标记物的三维分析表明,上皮细胞极性在小管形成过程中短暂丧失,随后恢复。此外,细胞间连接复合物的成分发生了深刻的重排:E-钙黏蛋白随机分布在细胞表面,桥粒斑蛋白I/II在细胞内积累,紧密连接蛋白ZO-1仍定位在细胞间接触位点。这表明细胞间连接的差异调节对小管的形成很重要。因此,在小管形成过程中,细胞间黏附接触受到差异调节,而质膜亚结构域的极性和特化则进行重组,使细胞在重排成新结构时能够保持接触。

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