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.

中文翻译：

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肌动蛋白依赖性胶原蛋白对内皮芽的侵袭。

在萌芽过程中，血管生成（现有血管中血管的生长）中的内皮细胞（EC）采用细长的侵入形式，并在细胞与细胞以及细胞与基质的相互作用部位施加作用力。这些细胞形状的改变和细胞的牵引力要求放线菌素网络的广泛重组。然而，肌动蛋白和肌球蛋白在内皮发芽中的各自作用尚未完全阐明。在这项研究中，我们通过用针对肌球蛋白或肌动蛋白的化合物治疗2D迁移和3D发芽的EC来进一步研究这些作用。这些治疗方法以化合物特异性的方式极大地影响了内皮细胞骨架并降低了侵袭性反应。指向在发芽期间严格控制肌动蛋白和肌球蛋白的活性。数据中的簇进一步说明了内皮发芽形态对体外模型机械微环境敏感，并将未来的研究引向机械底物指导，以作为促进工程组织血管化的策略。总而言之，我们的结果增加了研究的范围，突出了细胞骨架在发芽血管生成中的关键作用。