Sheng-Jun Cao1, Lei Hong2, Xiao-Qiang Li3. 1. Department of Vascular Surgery, Taizhou Second People's Hospital, Jiangsu, China. 2. Department of The First Affiliated Hospital of USTC, Anhui, China. 3. Department of Vascular Surgery, Nanjing Drum Tower Hospital, Jiangsu, China.
Abstract
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.
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.