Angiogenesis, the formation of new vessels, occurs in both developmental and pathological contexts. Prior research has investigated vessel formation to identify cellular phenotypes and dynamics associated with angiogenic disease. One major family of proteins involved in angiogenesis are the Rho GTPases, which govern function related to cellular elongation, migration, and proliferation. Using a mechanochemical model coupling Rho GTPase activity and cellular and intercellular mechanics, we investigate the role of cellular mitosis on sprouting angiogenesis. Mitosis-GTPase synchronization was not a strong predictor of GTPase and thus vessel signaling instability, whereas the location of mitotic events was predicted to alter GTPase cycling instabilities. Our model predicts that middle stalk cells undergoing mitosis introduce irregular dynamics in GTPase cycling and may provide a source of aberrant angiogenesis. We also find that cellular and junctional tension exhibit spatial heterogeneity through the vessel, and that tension feedback, specifically in stalk cells, tends to increase the maximum forces generated in the vessel.

血管生成，即新血管的形成，发生在发育和病理环境中。先前的研究已经调查了血管形成，以确定与血管生成疾病相关的细胞表型和动力学。参与血管生成的一个主要蛋白质家族是 Rho GTPases，它控制与细胞伸长、迁移和增殖相关的功能。使用耦合 Rho GTPase 活性和细胞和细胞间力学的机械化学模型，我们研究了细胞有丝分裂对发芽血管生成的作用。有丝分裂-GTPase 同步不是 GTPase 的强预测因子，因此血管信号不稳定性，而预测有丝分裂事件的位置会改变 GTPase 循环不稳定性。我们的模型预测，经历有丝分裂的中茎细胞会在 GTPase 循环中引入不规则的动力学，并可能提供异常血管生成的来源。我们还发现细胞和连接张力通过血管表现出空间异质性，并且张力反馈，特别是在茎细胞中，往往会增加血管中产生的最大力。