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Actomyosin-dependent invasion of endothelial sprouts in collagen

机译:胶原蛋白依赖于内皮芽的侵入性侵袭

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摘要

During sprouting angiogenesis-the growth of blood vessels from the existing vasculature-endothelial cells (ECs) adopt an elongated invasive form and exert forces at cell-cell and cell-matrix interaction sites. These cell shape changes and cellular tractions require extensive reorganizations of the actomyosin network. However, the respective roles of actin and myosin for endothelial sprouting are not fully elucidated. In this study, we further investigate these roles by treating 2D-migrating and 3D-sprouting ECs with chemical compounds targeting either myosin or actin. These treatments affected the endothelial cytoskeleton drastically and reduced the invasive response in a compound-specific manner; pointing toward a tight control of the actin and myosin activity during sprouting. Clusters in the data further illustrate that endothelial sprout morphology is sensitive to the in vitro model mechanical microenvironment and directs future research toward mechanical substrate guidance as a strategy for promoting engineered tissue vascularization. In summary, our results add to a growing corpus of research highlighting a key role of the cytoskeleton for sprouting angiogenesis.
机译:在发芽血管生成期间 - 来自现有脉管系统 - 内皮细胞(ECS)的血管的生长采用细长的侵入形式并在细胞 - 细胞和细胞 - 基质相互作用位点施加力。这些细胞形状的变化和细胞诉讼需要广泛重组的肌动酶网络。然而,肌动蛋白和肌球蛋白对内皮发芽的各自作用尚未完全阐明。在这项研究中,我们通过用靶向肌蛋白或肌动蛋白的化学化合物治疗2D迁移和3D发芽EC来进一步研究这些作用。这些治疗在急剧上影响内皮细胞骨架,并以复合特异性方式降低了侵入性反应;指向在发芽过程中对肌动蛋白和肌球蛋白活动的紧密控制。数据中的簇进一步说明内皮萌芽形态对体外模型机械微环境敏感,并将未来的机械基板引导研究引导为促进工程组织血管化的策略。总之,我们的结果增加了越来越多的研究语料库,突出了细胞骨架用于发芽血管生成的关键作用。

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