转录因子细胞启动子 2 是上游结合蛋白 1 介导的血管生成所必需的。
Transcription factor cellular promoter 2 is required for upstream binding protein 1 -mediated angiogenesis.
机构信息
Department of Neurology, Liaocheng Third People's Hospital, No. 62 Weiyu Road, Dongchangfu District, Liaocheng, Shandong, 252000, China.
The Second Department of Neurology, Gaotang People's Hospital, North of Provincial Road No.520 and West of Binhu Road, Gaotang County, Liaocheng, Shandong, 252800, China.
出版信息
Gene Expr Patterns. 2023 Jun;48:119308. doi: 10.1016/j.gep.2023.119308. Epub 2023 Mar 6.
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.
目的
血管生成是修复组织损伤的关键过程，其受到抗血管生成因子的精细平衡调节。在本研究中，我们研究了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 Western blot（WB）检测人脐静脉内皮细胞（HUVEC）中 UBP1 和 TFCP2 的水平。通过在基质胶测定和划痕测定中检测 UBP1 对血管生成和迁移的影响。通过 STRING 和共免疫沉淀（Co-IP）预测和验证 UBP1 与 TFCP2 之间的相互作用。
结果
首先，在 HUVECs 中血管内皮生长因子（VEGF）的刺激下，UBP1 的表达水平上调，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 HUVECs 中 TFCP2 的表达水平上调。此外，在 VEGF 刺激的 HUVECs 中，TFCP2 的敲低抑制了血管生成和迁移，而 UBP1 的下调增强了抑制作用。
结论
TFCP2 也在 VEGF 刺激的 HUVECs 中 UBP1 介导的血管生成中发挥关键作用。这些发现将为治疗血管生成性疾病提供新的理论基础。
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