Correlations of iodide ions with vascular endothelial growth factor and its receptors during the proliferation of vascular endothelial cells

Teng, Fei; Zu, Maoheng; Hua, Qian

doi:10.4238/2014.august.25.7

Cited by 3 publications

(4 citation statements)

References 15 publications

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“…It was found that at iodine concentration of 300-500 μg/l, the proliferation of vascular endothelial cells and hyperplasia of fibroblasts can be induced. It is speculated that high iodine concentration can lead to vascular endothelial cell proliferation [57,58]. Our study of the inferior vena cava septum revealed that the vascular endothelium of the inferior vena cava gradually thickened and merged into a septum.…”

Section: Iodine and Vascular Endothelial Proliferationmentioning

confidence: 76%

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Venous Interventions: From Lower-Limb Deep Vein Thrombosis to May-Thurner Syndrome and Budd-Chiari Syndrome

Wu¹,

Chen²,

Xu³

et al. 2020

Embolic Diseases - Evolving Diagnostic and Management Approaches

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Over the past decade, there have been great innovations in the diagnosis of venous disorder since the introduction of dual-source computed tomography (DSCT) in 2006. It provides fast and reliable diagnosis of deep vein thrombosis (DVT) with the capability of full leveling of thrombus burden and allows early endovascular interventions with pharmacomechanical aspiration thrombectomy (PMAT) being performed aiming to reduce the post-thrombotic syndrome (PTS) and improve quality of life. The newly introduced ultrafast clot removal system, in patients who failed with PMAT, AngioJet, and EKOS, aids in rapid restoration of venous flow and decline of venous hypertension to mitigate the valve damage. Percutaneous transluminal angioplasty (PTA) and stenting yield high technical success rate of 93-96% and a promising short-term 1-year and 2-year patency of around 93% and 75-79%, respectively, for symptomatic May-Thurner syndrome (MTS). Based on the cumulative endovascular treatment experience in over 2000 cases in Xizou, China, some relevant precipitating factors are addressed, and a new classification of subtypes have been proposed to guide the proper selection of endovascular management of Budd-Chiari syndrome (BCS).

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Section: Iodine and Vascular Endothelial Proliferationmentioning

confidence: 76%

“…Statistical analysis of 2406 patients found that the proportion of hepatic vein occlusion in adolescents under 30 years of age was significantly higher than in patients over 30 years of age [55,56]. The proportion of inferior vena cava obstruction increases with increasing age in patients aged 30-79 years old.…”

Section: Etiologymentioning

confidence: 99%

Venous Interventions: From Lower-Limb Deep Vein Thrombosis to May-Thurner Syndrome and Budd-Chiari Syndrome

Wu¹,

Chen²,

Xu³

et al. 2020

Embolic Diseases - Evolving Diagnostic and Management Approaches

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show abstract

“…However, MOVC is the most prevalent among all types of BCS in China 19 . Reports show that the surface of the inferior vena cava septum covered with endothelial cells, and vascular endothelial tissues are the main ingredients on the surface of the membrane 20 . Therefore, the abnormal proliferation and angiogenesis of HUVECs are the key factors involved in membranous formation.…”

Section: Discussionmentioning

confidence: 99%

Extracellular vesicles‐transmitted long non‐coding RNA MTUS2‐5 promotes proliferation and vascularization of human vascular endothelial cells in patients with Budd–Chiari syndrome

Zhang,

Feng,

Zhou

et al. 2023

J Cellular Molecular Medi

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The high rates of misdiagnosis and untreated mortality with regard to Budd–Chiari syndrome (BCS) indicated the need to screen effective biomarkers. The aim of this study was to explore the function of extracellular vesicles (EVs) in patients with BCS as well as associated mechanisms. First, differentially expressed long non‐coding RNAs (lncRNAs) from EVs separated from serum between BCS and healthy controls were screened using microarray analysis. Second, the proliferation, migration and tube formation of human vascular endothelial cells (HUVECs) were detected after EVs treatment, along with vascular endothelial growth factor (VEGF) levels and inflammatory factors from the cell supernatant. Last, the overexpressed lncRNA was transfected into the cells to further explore the mechanisms involved. Extracellular vesicles of BCS patients have significantly higher levels of lncRNA MTUS2‐5 than healthy controls. Apparently, treatment with EVs from BCS or the ones transfected with plasmids that overexpress lncRNA MTUS2‐5 enhances proliferation, migration and angiogenesis capacity. The results were considerably better than those obtained from treatment with EVs from healthy controls or transfection with the normal control plasmid, which also elevated the level of VEGF and inflammatory factors. Furthermore, FOS and PTGS2 were potentially regulated by the lncRNA MTUS2‐5 transmitted by EVs. The lncRNA MTUS2‐5 in EVs plays an important role in angiogenesis in the Budd–Chiari syndrome.

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“…Riemens et al (22) reported that the inferior vena cava septum is composed of small pieces of fibrous tissue, which contain capillaries, and the surface is covered with endothelial cells. The two surfaces of the membrane are composed of vascular endothelial tissues and membrane formation occurs due to endothelial damage (4,23). Therefore, abnormal proliferation and angiogenesis of HUVECs are the key factors involved in membranous formation.…”

Section: Discussionmentioning

confidence: 99%

miR‑3133 inhibits proliferation and angiogenesis by targeting the JUNB/VEGF pathway in human umbilical vein endothelial cells

Cao

Zhang

et al. 2020

Oncol Rep

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Membranous obstruction of the inferior vena cava (MOVC) has the highest incidence rate among the different types of Budd-Chiari syndrome (BCS) in China. The inferior vena cava septum of patients with MOVC contains capillaries and the two surfaces of the membrane are composed of vascular endothelial tissue. Membrane formation occurs due to endothelial damage. MicroRNAs (miRNAs/miRs) have been verified to be involved in the pathogenesis and progression of various human diseases. A previous study by our group suggested that miR-3133 was downregulated in the serum of patients with MOVC. In the present study, the possible mechanistic implication of miR-3133 in MOVC-associated processes was further explored. It was observed that miR-3133 overexpression inhibited, whereas miR-3133 knockdown enhanced the proliferation and tube formation of human umbilical vein endothelial cells (HUVECs) using the CCK-8 and tube formation assays. JUNB, a member of activator protein 1 and an important upstream transcriptional molecule of vascular endothelial growth factor (VEGF), was proven to be a direct target gene of miR-3133 using a bioinformatics prediction and luciferase reporter assay. Meanwhile, the mRNA and protein expression of JUNB and VEGF was determined by PCR, ELISA and western blot analyses. Of note, miR-3133 overexpression downregulated, while miR-3133 knockdown elevated the expression of JUNB and VEGF significantly. Furthermore, it was demonstrated that JUNB upregulated the expression and secretion of VEGF to promote HUVEC proliferation and angiogenesis. miR-3133 was able to inhibit the effect of JUNB overexpression to promote cell proliferation, angiogenesis and the expression of VEGF. In conclusion, the present study demonstrated that miR-3133 regulated endothelial cell proliferation and angiogenesis through the JUNB/VEGF pathway, which may provide an approach for inhibiting diaphragm formation of the inferior vena cava in MOVC.

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Correlations of iodide ions with vascular endothelial growth factor and its receptors during the proliferation of vascular endothelial cells

Cited by 3 publications

References 15 publications

Venous Interventions: From Lower-Limb Deep Vein Thrombosis to May-Thurner Syndrome and Budd-Chiari Syndrome

Venous Interventions: From Lower-Limb Deep Vein Thrombosis to May-Thurner Syndrome and Budd-Chiari Syndrome

Extracellular vesicles‐transmitted long non‐coding RNA MTUS2‐5 promotes proliferation and vascularization of human vascular endothelial cells in patients with Budd–Chiari syndrome

miR‑3133 inhibits proliferation and angiogenesis by targeting the JUNB/VEGF pathway in human umbilical vein endothelial cells

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