通过 EMT 探讨 TGF-β1 在血管生成中的作用机制。
Mechanistic studies on the role of TGF-β1 in angiogenesis through EndMT.
机构信息
Department of Vascular Surgery, Taizhou Second People's Hospital, Jiangsu, China.
Department of The First Affiliated Hospital of USTC, Anhui, China.
出版信息
Vascular. 2021 Jun;29(3):442-450. doi: 10.1177/1708538120953668. Epub 2020 Oct 9.
OBJECTIVE
This study aims to investigate the mechanism of transforming growth factor-β1 (TGF-β1) in promoting angiogenesis through endothelial-to-mesenchymal transition (EndMT).
METHODS
The mesenchymal transition of human umbilical vein endothelial cells (HUVECs) was induced by TGF-β1. The angiogenesis, migration, and proliferation of HUVECs undergoing EndMT were examined by tube formation assay, scratch assay, Transwell assay, and CCK-8 assay.
RESULTS
The outcomes revealed that EndMT promoted angiogenesis, migration, and proliferation of HUVECs and the secretion of the vascular endothelial growth factor (VEGF) of HUVECs. Phosphorylated AKT (p-AKT) increased in EndMT by inhibiting the mitigation of angiogenesis.
CONCLUSION
EndMT induces angiogenesis by promoting the secretion of VEGF, and p-AKT participates in this regulation.
目的
本研究旨在探讨转化生长因子-β1（TGF-β1）通过内皮细胞向间充质转化（EndMT）促进血管生成的机制。
方法
用 TGF-β1 诱导人脐静脉内皮细胞（HUVEC）的间质转化。通过管形成试验、划痕试验、Transwell 试验和 CCK-8 试验检测经历 EndMT 的 HUVEC 的血管生成、迁移和增殖。
结果
结果表明，EndMT 促进 HUVEC 的血管生成、迁移和增殖，以及 HUVEC 血管内皮生长因子（VEGF）的分泌。通过抑制血管生成的缓解，EndMT 中磷酸化 AKT（p-AKT）增加。
结论
EndMT 通过促进 VEGF 的分泌诱导血管生成，p-AKT 参与这种调节。
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