Objective

Angiogenesis is a key process of repairing tissue damage, and it is regulated by the delicate balance between anti-angiogenesis factors. In the present study, we investigate whether transcription factor cellular promoter 2 (TFCP2) is required for upstream binding protein 1 (UBP1)-mediated angiogenesis.

Methods

Levels of UBP1 and TFCP2 in human umbilical vein endothelial cells (HUVECs) are detected by quantitative polymerase chain reaction (q-PCR) and Western blotting (WB). Effects of UBP1 on angiogenesis and migration are detected by tube-like network formation on matrigel assay and scratch assay. The interaction between UBP1 and TFCP2 is predicted and verified by STRING and Co-immunoprecipitation (Co-IP).

Results

Firstly, the UBP1 expression level was up-regulated in the stimuli of vascular endothelial growth factor (VEGF) in HUVECs, and the knockdown of UBP1 inhibited angiogenesis and migration of HUVECs. Then, UBP1 interacted with TFCP2. Besides, the TFCP2 expression level was up-regulated in VEGF-stimulated HUVECs. Furthermore, knockdown of TFCP2 inhibited angiogenesis and migration in VEGF-stimulated HUVECs, and down-regulation of UBP1 enhanced the inhibition.

Conclusion

TFCP2 also plays a key role in UBP1 mediated angiogenesis of HUVECs stimulated by VEGF. These findings will provide a new theoretical basis for the treatment of angiogenic diseases.

中文翻译：

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上游结合蛋白 1 介导的血管生成需要转录因子细胞启动子 2

客观的

血管生成是修复组织损伤的关键过程，它受到抗血管生成因子之间微妙平衡的调节。在本研究中，我们研究转录因子细胞启动子 2 (TFCP2) 是否是上游结合蛋白 1 (UBP1) 介导的血管生成所必需的。

方法

通过定量聚合酶链反应（q-PCR）和蛋白质印迹（WB）检测人脐静脉内皮细胞（HUVEC）中UBP1和TFCP2的水平。通过基质胶实验和划痕实验中管状网络的形成来检测UBP1对血管生成和迁移的影响。UBP1 和 TFCP2 之间的相互作用通过 STRING 和免疫共沉淀 (Co-IP) 进行预测和验证。

结果

首先，HUVECs中UBP1的表达水平在血管内皮生长因子（VEGF）的刺激下上调，并且UBP1的敲低抑制了HUVECs的血管生成和迁移。然后，UBP1与TFCP2相互作用。此外，在 VEGF 刺激的 HUVEC 中 TFCP2 表达水平上调。此外，敲低 TFCP2 会抑制 VEGF 刺激的 HUVEC 中的血管生成和迁移，而下调 UBP1 会增强这种抑制作用。

结论

TFCP2 在 VEGF 刺激的 UBP1 介导的 HUVEC 血管生成中也发挥着关键作用。这些发现将为血管生成性疾病的治疗提供新的理论基础。