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首页> 外文期刊>Glia >Impaired intercellular adhesion and immature adherens junctions in merlin-deficient human primary schwannoma cells
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Impaired intercellular adhesion and immature adherens junctions in merlin-deficient human primary schwannoma cells

机译：merlin缺陷的人类原发性神经鞘瘤细胞中细胞间粘附和未成熟的粘附连接受损

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摘要

Schwannomas that occur spontaneously or in patients with neurofibromatosis Type 2, lack both alleles for the tumor suppressor and plasma membrane-cytoskeleton linker merlin. We have shown that human primary schwannoma cells display activation of the RhoGTPases Rac1 and Cdc42 which results in highly dynamic and ongoing protrusive activity like ruffling. Ruffling is an initial and temporally limited step in the formation of intercellular contacts like adherens junctions that are based on the cadherin-catenin system. We tested if there is a connection between Rac1-induced ongoing ruffling and the maintenance, stabilization and functionality of adherens junctions and if this is of relevance in human, merlin-deficient schwannoma cells. We show intense ongoing ruffling is not limited to membranes of single human primary schwannoma cells, but occurs also in membranes of contacting cells, even when confluent. Live cell imaging shows that newly formed contacts are released after a short time, suggesting disturbed formation or stabilization of adherens junctions. Morphology, high phospho-tyrosine levels and cortactin staining indicate that adherens junctions are immature in human primary schwannoma cells, whereas they display characteristics of mature adherens junctions in human primary Schwann cells. When merlin is reintroduced, human primary schwannoma cells show only initial ruffling in contacting cells and adherens junctions appear more mature. We therefore propose that ongoing Rac-induced ruffling causes immature adherens junctions and leads to impaired, nonfunctional intercellular adhesion in aggregation assays in merlin-deficient schwannoma cells that could be an explanation for increased proliferation rates due to loss of contact inhibition or tumor development in general. (C) 2008 Wiley-Liss, Inc.
机译：自发性或在2型神经纤维瘤病患者中发生的神经鞘瘤缺乏用于肿瘤抑制因子的等位基因和质膜-细胞骨架接头merlin。我们已经表明，人类原发性神经鞘瘤细胞显示RhoGTPases Rac1和Cdc42的激活，从而导致高动态性和进行性的活动，如皱纹。在基于钙粘蛋白-连环蛋白系统的细胞间接触（如粘附连接）形成过程中，波纹作用是一个初始且在时间上受限制的步骤。我们测试了Rac1诱导的持续性波动与粘附连接的维持，稳定和功能之间是否存在联系，以及这是否与人，缺乏merlin的神经鞘瘤细胞有关。我们显示出激烈的持续性波动不仅限于单个人类原发性神经鞘瘤细胞的膜，而且甚至在接触细胞的膜中也发生，即使在融合时也是如此。活细胞成像显示，新形成的触点在短时间内释放，表明粘附连接的形成或稳定。形态，高磷酸酪氨酸水平和cortactin染色表明，黏附连接在人类原发性神经鞘瘤细胞中不成熟，而它们在人类原发性施旺细胞中表现出成熟的黏附连接特征。重新引入merlin后，人原发性神经鞘瘤细胞仅在接触细胞中起初起伏，粘附连接似乎更成熟。因此，我们建议进行中的Rac诱导的起皱会导致不成熟的粘附连接，并导致在缺乏merlin的神经鞘瘤细胞的聚集测定中受损的，非功能性的细胞间粘附，这可能是由于失去接触抑制或肿瘤发展而导致增殖率增加的一种解释。 （C）2008 Wiley-Liss，Inc.

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