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首页> 外文期刊>Endothelium: Journal of endothelial cell research >B1 integrin activation inhibits in vitro tube formation: effects on cell migration, vacuole coalescence and lumen formation.
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B1 integrin activation inhibits in vitro tube formation: effects on cell migration, vacuole coalescence and lumen formation.

机译：B1整联蛋白激活抑制体外管形成：对细胞迁移，液泡聚结和管腔形成的影响。

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Human endothelial cells (EC), when plated onto gels of extracellular matrix proteins such as Matrigel or collagen form capillary tubes in a process thought to mimic angiogenesis. We have shown previously that the extent of tube formation and the phenotype of the lumen are regulated by integrins (Gamble et al 1993) and lumen formation occurs through a process of vacuolization, coalescence and ultimate directional fusion of these vacuoles with the plasma membrane (Meyer 1997 et al). We now show here that activation of beta1 integrins on endothelial cells inhibits tube formation. On collagen gels, endothelial cells treated with 31 activating antibody 8A2 failed to migrate into the gel and tube formation was inhibited. Although several integrins mediate EC attachment to collagen alpha2beta1 is the chief determinant of EC behaviour since a blocking antibody to (alpha2beta1 reversed the effect of 8A2. On Matrigel tube formation was also inhibited by 8A2 treatment although cell alignment and sprout formation was still evident. Electron microscopy revealed the organisation of normal numbers of cells into solid sprouts and the formation of small intracellular vacuoles suggesting that initial stages of tube formation including cell migration were unaffected. However, beta1 integrin activation inhibited the coalescence of these small vacuoles into larger vacuoles, the recruitment of more cells into the sprout and the subsequent formation of mature lumen. The inhibition of capillary tube formation by beta1 activation was time dependent and long lasting. The critical time for activation of the beta1 integrin was the initial 1-2h after plating in order to inhibit tube formation although once activated, the beta1 mediated inhibition on Matrigel was still evident 4 days later. Our results suggest that beta1 integrins are critical in capillary tube formation in at least two phases. beta1 integrins are essential for migration of EC through collagen gels. Independently, beta1 integrins, although not involved in initial vacuole formation, are involved in the process of vacuole coalescence and subsequent lumen formation since beta1 integrin activation inhibits these processes.
机译：当人类内皮细胞（EC）涂在细胞外基质蛋白（如Matrigel或胶原蛋白）的凝胶上时，会形成毛细管，被认为是模仿血管生成的过程。先前我们已经表明，管形成的程度和管腔的表型由整联蛋白调节（Gamble et al 1993），并且管腔的形成是通过这些液泡与质膜（Meyer）的空泡化，聚结和最终定向融合的过程发生的。 1997等）。现在我们在这里显示，内皮细胞上的beta1整合素的激活抑制了管的形成。在胶原蛋白凝胶上，用31种活化抗体8A2处理的内皮细胞无法迁移到凝胶中，并且抑制了管的形成。尽管几种整合素介导EC对胶原蛋白alpha2beta1的附着是EC行为的主要决定因素，因为针对（alpha2beta1的阻断抗体）逆转了8A2的作用。尽管细胞排列和发芽形成仍然很明显，但8A2处理也抑制了Matrigel管的形成。显微镜检查显示正常数目的细胞组织成固体芽，并形成小的细胞内液泡，这表明试管形成的初始阶段（包括细胞迁移）不受影响，但是，β1整合素的活化抑制了这些小液泡聚集成较大的液泡，更多的细胞进入萌芽并随后形成成熟的内腔。β1激活对毛细管形成的抑制作用是时间依赖性和持久的。β1整联蛋白激活的关键时间是接种后最初的1-2h。阻止管子形成，尽管一旦激活，下注4天后，a1介导的对Matrigel的抑制仍然明显。我们的结果表明，beta1整合素在至少两个阶段的毛细管形成中至关重要。 beta1整合素对于EC通过胶原蛋白凝胶的迁移至关重要。独立地，尽管β1整联蛋白不参与最初的液泡形成，但是由于β1整联蛋白的活化抑制了这些过程，因此参与了液泡聚结和随后的管腔形成的过程。

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