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首页> 外文期刊>Journal of Cellular Physiology >Zebrafish Tmem230a cooperates with the Delta/Notch signaling pathway to modulate endothelial cell number in angiogenic vessels
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Zebrafish Tmem230a cooperates with the Delta/Notch signaling pathway to modulate endothelial cell number in angiogenic vessels

机译:斑马鱼Tmem230a合作与δ/等级信号通路调节内皮细胞在血管生成血管

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摘要

During embryonic development, new arteries, and veins form from preexisting vessels in response to specific angiogenic signals. Angiogenic signaling is complex since not all endothelial cells exposed to angiogenic signals respond equally. Some cells will be selected to become tip cells and acquire migration and proliferation capacity necessary for vessel growth while others, the stalk cells become trailer cells that stay connected with pre‐existing vessels and act as a linkage to new forming vessels. Additionally, stalk and tip cells have the capacity to interchange their roles. Stalk and tip cellular responses are mediated in part by the interactions of components of the Delta/Notch and Vegf signaling pathways. We have identified in zebrafish, that the transmembrane protein Tmem230a is a novel regulator of angiogenesis by its capacity to regulate the number of the endothelial cells in intersegmental vessels by co‐operating with the Delta/Notch signaling pathway. Modulation of Tmem230a expression by itself is sufficient to rescue improper number of endothelial cells induced by aberrant expression or inhibition of the activity of genes associated with the Dll4/Notch pathway in zebrafish. Therefore, Tmem230a may have a modulatory role in vessel‐network formation and growth. As the Tmem230 sequence is conserved in human, Tmem230 may represent a promising novel target for drug discovery and for disease therapy and regenerative medicine in promoting or restricting angiogenesis.
机译:在胚胎发育期间,新的动脉,静脉形成从先前存在的血管反应特定的血管生成信号。并不是所有的内皮以来信号是复杂的细胞暴露于血管生成信号做出反应同样。提示细胞和获得迁移和扩散生长所必需的能力其他人,茎细胞成为拖车的细胞保持联系与提前现有船只和行动作为一个链接到新血管形成。此外,茎尖细胞交换他们的角色的能力。提示细胞反应介导的组件的交互的δ/等级和Vegf信号通路。在斑马鱼,跨膜蛋白Tmem230a是一种新型的监管机构的血管生成其调节的数量的能力在节间血管内皮细胞公司运营与δ/ Notch信号途径。本身就足以拯救不当的数量异常引起的内皮细胞表达或抑制相关基因的活动在斑马鱼Dll4 / Notch通路。因此,Tmem230a可能有调节作用船舶网络的形成和发展。Tmem230 Tmem230序列是守恒的人类可能代表一种很有前途的新型药物的目标发现和疾病治疗再生医学在促进或限制血管生成。

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