The TGF-β1 Induces the Endothelial-to-Mesenchymal Transition via the UCA1/miR-455/ZEB1 Regulatory Axis in Human Umbilical Vein Endothelial Cells

2020 ◽  
Vol 39 (7) ◽  
pp. 1264-1273
Author(s):  
Ying Zhang ◽  
Kun Fan ◽  
Xiaotao Xu ◽  
Aizhong Wang
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Mesenchymal Transition ◽  
Human Umbilical Vein ◽  
Endothelial To Mesenchymal Transition ◽  
Umbilical Vein Endothelial Cells ◽  
Tgf Β1

scholarly journals CXCR7 Inhibits Fibrosis via Wnt/β-Catenin Pathways during the Process of Angiogenesis in Human Umbilical Vein Endothelial Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
MinQian Shen ◽  
YiFan Feng ◽  
Jing Wang ◽  
YuanZhi Yuan ◽  
Fei Yuan
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Tube Formation ◽  
Erk Signaling ◽  
Cell Type ◽  
Mesenchymal Transition ◽  
Human Umbilical Vein ◽  
Endothelial To Mesenchymal Transition ◽  
Umbilical Vein Endothelial Cells ◽  
Tissue Origin

Although SDF-1/CXCR7 plays an important role in angiogenesis, the function and the pathway of the SDF-1/CXCR7 axis might depend on the cell type or tissue origin and not fully understood. In this study, we investigated the effect of CXCR7 in SDF-1-induced proliferation, migration, apoptosis, tube formation, and endothelial-to-mesenchymal transition (EndMT) of human umbilical vein endothelial cells (HUVECs), and the potential pathway of SDF-1/CXCR7. We confirmed that the silencing of CXCR7 inhibited the proliferation of HUVECs and contributed the apoptosis, while overexpressed CXCR7 increased SDF-1-induced HUVECs migration and tube formation. However, upregulated CXCR7 inhibited the expression of α-SMA, suggesting that CXCR7 might attenuate EndMT. In addition, overexpressed CXCR7 activated AKT and ERK signaling pathways but suppressed Wnt/β-catenin pathways in HUVECs. The inhibition of Wnt/β-catenin pathways decreased the expression of α-SMA. Altogether, these results suggest that CXCR7 might inhibit fibrosis via Wnt/β-catenin pathways during the process of angiogenesis.

scholarly journals MiR-200c-3p promotes ox-LDL-induced endothelial to mesenchymal transition in human umbilical vein endothelial cells through SMAD7/YAP pathway

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Yongzhong Mao ◽  
Ling Jiang
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Critical Role ◽  
Luciferase Reporter ◽  
Rhodamine Phalloidin ◽  
Mesenchymal Transition ◽  
Human Umbilical Vein ◽  
Endothelial To Mesenchymal Transition ◽  
Umbilical Vein Endothelial Cells

Abstract Background Endothelial to mesenchymal transition (EndMT) participates in the progression of atherosclerosis (AS). MiR-200c-3p has been implicated in EndMT. However, the functional role of miR-200c-3p in AS remains largely unknown. Here, we demonstrated the critical role of miR-200c-3p in regulating EndMT in AS. Methods ApoE−/− mice were fed with high-fat diet to establish AS mouse model, and human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) to mimic AS cell model. The expression of miR-200c-3p, SMAD7 and YAP in ApoE−/− mice and HUVECs was detected by quantitative real-time PCR. Rhodamine phalloidin staining and Western blot were performed to observe cell morphology and EndMT marker expression of HUVECs. Luciferase reporter assay and Co-Immunoprecipitation were performed to verify the relationship among miR-200c-3p, SMAD7, and YAP. Results MiR-200c-3p was highly expressed, and SMAD7 and YAP were down-regulated in the aortic tissues of ApoE−/− mice and ox-LDL-treated HUVECs. MiR-200c-3p overexpression promoted the transformation of ox-LDL-treated HUVECs from cobblestone-like epithelial phenotype to a spindle-like mesenchymal phenotype. Meanwhile, miR-200c-3p up-regulation repressed the expression of endothelial markers CD31 and vWF and promoted the expression of mesenchymal markers α-SMA and vimentin in the ox-LDL-treated HUVECs. MiR-200c-3p inhibited SMAD7 and YAP expression by interacting with 3′ untranslated region of SMAD7. Moreover, miR-200c-3p promoted EndMT in ox-LDL-treated HUVECs by inhibiting SMAD7/YAP pathway. Conclusion This work demonstrated that MiR-200c-3p promoted ox-LDL-induced EndMT in HUVECs through SMAD7/YAP pathway, which may be important for the onset of atherosclerosis.

Transforming Growth Factor Betal and Beta2 Induce Down-Modulation of Thrombomodulin in Human Umbilical Vein Endothelial Cells

1995 ◽  
Vol 73 (05) ◽  
pp. 812-818 ◽  
Author(s):  
Taro Ohji ◽  
Hajime Urano ◽  
Akira Shirahata ◽  
Minoru Yamagishi ◽  
Ken Higashi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Time Course ◽  
Transforming Growth Factor ◽  
Umbilical Vein ◽  
Mrna Levels ◽  
Antigen Level ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Tgf Β1

SummaryTo investigate the effects of transforming growth factor-betas (TGF-βs) on endothelial anticoagulant activity, we assayed thrombomodulin (TM) activity and antigen levels of human umbilical vein endothelial cells (HUVECs) incubated with TGF-βs in vitro. TGF-β1 suppressed surface TM activity and surface TM antigen levels maximally 12 h after incubation in dose-dependent manners. TGF-β2 was almost equipotent with TGF-β1 for the suppression of them. Both TGF-βs suppressed total TM antigen level in HUVECs, and the time course of the suppression was similar to that of the cell surface TM antigen level. The maximal reductions of TM mRNA levels by TGF-βs were observed at several hours ahead of those observed in both surface and total TM antigen levels, suggesting that the TGF-β-mediated suppression of TM antigen of HUVECs is primarily regulated at the TM mRNA level. Our present work suggests that the down-modulation of TM level induced by TGF-βs in HUVECs contributes in vivo to promoting the thrombogenesis either at the sites of injury of vessel walls, such as atherosclerotic lesions where TGF-β1 is released from platelets, smooth muscle cells and monocytes, or at neovascular walls in tumors secreting TGF-β2.

scholarly journals Effect of captopril on radiation-induced TGF-β1 secretion in EA.Hy926 human umbilical vein endothelial cells

Oncotarget ◽  
2017 ◽  
Vol 8 (13) ◽  
pp. 20842-20850 ◽  
Author(s):  
Jingni Wei ◽  
Hui Xu ◽  
Yinyin Liu ◽  
Baiyu Li ◽  
Fuxiang Zhou
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Radiation Induced ◽  
Umbilical Vein Endothelial Cells ◽  
Tgf Β1

Mechanistic studies on the role of TGF-β1 in angiogenesis through EndMT

Vascular ◽  
2020 ◽  
pp. 170853812095366
Author(s):  
Sheng-Jun Cao ◽  
Lei Hong ◽  
Xiao-Qiang Li
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Umbilical Vein ◽  
Transforming Growth Factor Β1 ◽  
Tube Formation ◽  
Mesenchymal Transition ◽  
Phosphorylated Akt ◽  
Endothelial To Mesenchymal Transition ◽  
Umbilical Vein Endothelial Cells ◽  
Tgf Β1

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.

scholarly journals Irradiated Human Umbilical Vein Endothelial Cells Undergo Endothelial-Mesenchymal Transition via the Snail/miR-199a-5p Axis to Promote the Differentiation of Fibroblasts into Myofibroblasts

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Minxiao Yi ◽  
Bo Liu ◽  
Yang Tang ◽  
Fang Li ◽  
Wan Qin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Smooth Muscle Actin ◽  
Lung Fibroblasts ◽  
Type I ◽  
Mesenchymal Transition ◽  
Human Umbilical Vein ◽  
Radiation Induced ◽  
Umbilical Vein Endothelial Cells ◽  
Endothelial Mesenchymal Transition

Radiation induced pulmonary fibrosis (RIPF) is one of the major side effects of radiotherapy for lung cancer. Previous studies have shown that endothelial cells and activated myofibroblasts play a key role in RIPF. However, the interaction between irradiated endothelial cells and activation of myofibroblasts has not been reported. The aim of the present study was to examine whether irradiated endothelial cells would affect the differentiation of fibroblasts into myofibroblasts in the process of RIPF. In the current study, we used a coculture system that allowed direct contact between human fetal lung fibroblasts (MRC-5) and irradiated human umbilical vein endothelial cells (HUVECs). After 24 or 48 h, cells were sorted by flow cytometry. Radiation induced endothelial-mesenchymal transition (EndMT) by significantly increasing the expression of Snail and vimentin and reducing the expression of CD31 in HUVECs. In addition, irradiation of HUVECs induced the expression of collagen type I and α-smooth muscle actin (α-SMA) in MRC-5 cells. Further investigation indicated that irradiation of HUVECs induced the differentiation of fibroblasts into myofibroblasts through the Snail/miR-199a-5p axis. We conclude that irradiated endothelial cells undergo EndMT to promote differentiation of fibroblasts into myofibroblasts via the Snail/miR-199a-5p axis.

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