scholarly journals Spatholobus suberectus extract suppresses proliferation and EMT, and promotes apoptosis in palmitic acid induced vascular endothelial cells by inhibiting LncRNA MALAT1 via VEGF signaling pathway

2020 ◽  
Vol 19 (5) ◽  
pp. 494-955
Author(s):  
Kebo Gu ◽  
Lili He
Keyword(s):  
Palmitic Acid ◽  
Signaling Pathway ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Mesenchymal Transition ◽  
Vegf Signaling ◽  
Lncrna Malat1 ◽  
Spatholobus Suberectus ◽  
Vegf Signaling Pathway

Purpose: In type 2 diabetes, palmitic acid could damage vessels and induce insulin resistance. This present in vitro study evaluates the possible role of Spatholobus suberectus (FSS) extract in diabetes.Methods: Human HUVECc cells were treated with palmitic acid, palmitic acid and Spatholobus suberectus extract. MALAT1 overexpression plasmid (pcDNA-MALAT1) and blank vector were transfected into the cells using lipofectamine 2000. RT-qPCR assay was used to evaluated the expression changes of lncRNA, VEGFR2 and VEGFA in the cells as well as Epithelial-Mesenchymal Transition (EMT) biomarkers and apoptosis. CCK-8 was used to detect cell viabilities of HUVECs. Expressions of proteins in VEGF signaling pathway were analyzed using Western Blot.Results: LncRNA MALAT1 had high expression in diabetes-like cells and suppressed proliferation and EMT but promoted apoptosis. The SS extract promoted proliferation and EMT and repressed apoptosis in diabetes-like HUVECs cells. The promotion of apoptosis by LncRNA MALAT1, inhibition of apoptosis and regulated functions of diabetes-like HUVECs cells by SS extract occurred via the VEGF signaling pathwayConclusion: SS extract might contribute to survival of cells by inhibiting MALAT1 via VEGF signaling pathway in vitro, suggesting FSF might be a potential therapeutic agent in the treatment of diabetes. Keywords: flavone of Spatholobus suberectus, diabetes, vascular endothelial cell, LncRNA MALAT1

scholarly journals The mTOR/AP-1/VEGF signaling pathway regulates vascular endothelial cell growth

Oncotarget ◽  
2016 ◽  
Vol 7 (33) ◽  
pp. 53269-53276 ◽  
Author(s):  
Shuo Wang ◽  
Jiawei Lu ◽  
Qingsheng You ◽  
Hua Huang ◽  
Yingying Chen ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Growth ◽  
Signaling Pathway ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Vegf Signaling ◽  
Endothelial Cell Growth ◽  
Vegf Signaling Pathway

scholarly journals DEPTOR Deficiency-Mediated mTORc1 Hyperactivation in Vascular Endothelial Cells Promotes Angiogenesis

2018 ◽  
Vol 46 (2) ◽  
pp. 520-531 ◽  
Author(s):  
Yan Ding ◽  
Lanlan Shan ◽  
Wenqing Nai ◽  
Xiaojun Lin ◽  
Ling Zhou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Gene Knockout ◽  
Umbilical Vein ◽  
Vascular Endothelial Cell ◽  
Tube Formation ◽  
Vascular Endothelial

Background/Aims: The mechanistic target of rapamycin (mTOR) signaling pathway is essential for angiogenesis and embryonic development. DEP domain-containing mTOR-interacting protein (DEPTOR) is an mTOR binding protein that functions to inhibit the mTOR pathway In vitro experiments suggest that DEPTOR is crucial for vascular endothelial cell (EC) activation and angiogenic responses. However, knowledge of the effects of DEPTOR on angiogenesis in vivo is limited. This study aimed to determine the role of DEPTOR in tissue angiogenesis and to elucidate the molecular mechanisms. Methods: Cre/loxP conditional gene knockout strategy was used to delete the Deptor gene in mouse vascular ECs. The expression or distribution of cluster of differentiation 31 (CD31), vascular endothelial growth factor (VEGF) and hypoxia inducible factor-1 alpha (HIF-1α) were detected by immunohistochemical staining or western blot. Tube formation assay was used to measure angiogenesis in vitro. Results: Deptor knockdown led to increased expression of CD31, VEGF and HIF-1α in heart, liver, kidney and aorta. After treatment with rapamycin, their expression was significantly down regulated. In vitro, human umbilical vein endothelial cells (HUVECs) were transfected with DEPTOR-specific small interfering RNA (siRNA), which resulted in a significant increase in endothelial tube formation and migration rates. In contrast, DEPTOR overexpression markedly reduced the expression of CD31, VEGF and HIF-1α. Conclusions: Our findings demonstrated that deletion of the Deptor gene in vascular ECs resulted in upregulated expression of CD31 and HIF-1α, and further stimulated the expression of VEGF which promoted angiogenesis, indicating that disruption of normal angiogenic pathways may occur through hyperactivation of the mTORC1/HIF-1α/VEGF signaling pathway.

scholarly journals Correlation between vascular endothelial growth factor pathway and immune microenvironment in head and neck squamous cell carcinoma

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chao Zhu ◽  
Liqun Gu ◽  
Zelong Liu ◽  
Jiang Li ◽  
Mianfeng Yao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Immune Cell ◽  
Vascular Endothelial ◽  
Related Gene ◽  
Immune Microenvironment ◽  
Vegf Signaling ◽  
Immune Related Gene ◽  
Tumor Immune Microenvironment ◽  
Endothelial Growth Factor ◽  
Vegf Signaling Pathway

Abstract Background Immunotherapy is a crucial therapeutic approach in oncology. However, most patients with head and neck squamous cell carcinoma (HNSCC) do not derive benefit from immunotherapy. Vascular endothelial growth factor (VEGF)/VEGF Receptor 2 (VEGFR2) signaling pathway is one of the most important pathways regulating angiogenesis in tumor. The combination of immunotherapy and anti-angiogenic therapy is considered to improve efficacy of immunotherapy. The correlation between VEGF signaling pathway and tumor immune microenvironment in HNSCC patients is unclear. Methods We utilized RNA sequencing and clinical data of HNSCC patients from the TCGA database to study the correlation between VEGF signaling pathway and tumor immune microenvironment, on aspect of immune cell infiltration, immune-related gene expression profiling and immune-related biological pathways. Results We observed that VEGF signaling pathway is positively correlated with immune cell infiltration, immune-related gene expression profiles, and the prognosis of HNSCC patients. The functional enrichment analysis of differentially expressed genes between different VEGF score subtypes detected multiple immune-related biological processes. Conclusion Our findings suggested that combining anti-VEGF signaling pathway agents with immunotherapy, such as immune checkpoint inhibitors (ICI) therapy, may exhibit encouraging benefits in HNSCC.

scholarly journals MicroRNA-183 inhibition exerts suppressive effects on diabetic retinopathy by inactivating BTG1-mediated PI3K/Akt/VEGF signaling pathway

2019 ◽  
Vol 316 (6) ◽  
pp. E1050-E1060 ◽  
Author(s):  
Zhen-Zhen Zhang ◽  
Xiu-Hong Qin ◽  
Jing Zhang
Keyword(s):  
Endothelial Cells ◽  
Diabetic Retinopathy ◽  
Cell Growth ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Vascular Endothelial Cells ◽  
Tube Formation ◽  
Vascular Endothelial ◽  
Vegf Signaling ◽  
Vegf Signaling Pathway

Diabetic retinopathy (DR) is a serious diabetic complication caused by both environmental and genetic factors. Molecular mechanisms of DR may lead to the discovery of reliable prognostic indicators. The current study aimed to clarify the mechanism of microRNA-183 (miR-183) in DR in relation to the PI3K/Akt/VEGF signaling pathway. Microarray-based gene expression profiling of DR was used to identify the differentially expressed genes. Sprague-Dawley rats were used for the establishment of DR models, and then miR-183 was altered by mimic or inhibitor or BTG1 was downregulated by siRNA to explore the regulatory mechanism of miR-183 in DR. Furthermore, the expression of miR-183, CD34, endothelial nitric oxide synthase (eNOS), BTG1 and the PI3K/Akt/VEGF signaling pathway-related genes as well as reactive oxygen species (ROS) level was determined, and the relationship between miR-183 and BTG1 was also verified. Cell growth, cell apoptosis, and angiogenesis were determined. Microarray analysis revealed the involvement of miR-183 in DR via the PI3K/Akt/VEGF signaling pathway by targeting BTG1. Upregulated miR-183 and downregulated BTG1 were observed in retinal tissues of DR rats. miR-183 overexpression activated the PI3K/Akt/VEGF signaling pathway, upregulated CD34, eNOS, and ROS, and inhibited BTG1. BTG1 was confirmed as a target gene of miR-183. miR-183 overexpression or BTG1 knockdown promoted cell growth and tube formation while it suppressed cell apoptosis of vascular endothelial cells in DR rats. In this study, we demonstrated that miR-183 silencing inhibiting cell growth and tube formation in vascular endothelial cells of DR rats via the PI3K/Akt/VEGF signaling pathway by upregulating BTG1.

scholarly journals PTEN inhibitor improves vascular remodeling and cardiac function after myocardial infarction through PI3k/Akt/VEGF signaling pathway

2020 ◽  
Vol 26 (1) ◽  
Author(s):  
Qiuting Feng ◽  
Xing Li ◽  
Xian Qin ◽  
Cheng Yu ◽  
Yan Jin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Signaling Pathway ◽  
Cardiomyocyte Apoptosis ◽  
Therapeutic Drug ◽  
Vascular Endothelial ◽  
Vegf Signaling ◽  
Endothelial Growth Factor ◽  
To Receive ◽  
Vegf Signaling Pathway

Abstract Background Myocardial infarction (MI) is the leading cause of death from cardiovascular disease (CVD). Currently, the efficacy for MI treatment remains unsatisfactory. Therefore, it is urgent to develop a novel therapeutic strategy. Methods Left anterior descending arteries (LAD) of mice were ligated to induce MI. Another set of mice were intravenously injected with PTEN inhibitor BPV (1 mg/kg) 1 h after LAD ligation and continued to receive BPV injection daily for the following 6 days. Mice were performed echocardiography 14 days after surgery. Results Mice in MI group displayed an increased expression of PTEN with impaired cardiac function, enhanced cardiomyocyte apoptosis and decreased angiogenesis. BPV treatment significantly improved cardiac function, with reduced cardiomyocyte apoptosis, promoted angiogenesis, and activated PI3K/Akt/vascular endothelial growth factor (VEGF) signaling pathway. Conclusion PTEN inhibitor BPV could effectively prevent myocardial infarction in mice, highlighting its potential as a candidate therapeutic drug.

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