scholarly journals Fumonisin B1 Inhibits Cell Proliferation and Decreases Barrier Function of Swine Umbilical Vein Endothelial Cells

Toxins ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 863
Author(s):  
Qing Li ◽  
Qiaoling Yuan ◽  
Tianjie Wang ◽  
Yang Zhan ◽  
Lingchen Yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Barrier Function ◽  
Umbilical Vein ◽  
Animal Health ◽  
Fumonisin B1 ◽  
Cyclin B1 ◽  
Sphingolipid Metabolism ◽  
Cyclin E1 ◽  
Umbilical Vein Endothelial Cells

The fumonisins are a group of common mycotoxins found around the world that mainly contaminate maize. As environmental toxins, they pose a threat to human and animal health. Fumonisin B1 (FB1) is the most widely distributed and the most toxic. FB1 can cause pulmonary edema in pigs. However, the current toxicity mechanism of fumonisins is still in the exploratory stage, which may be related to sphingolipid metabolism. Our study is designed to investigate the effect of FB1 on the cell proliferation and barrier function of swine umbilical vein endothelial cells (SUVECs). We show that FB1 can inhibit the cell viability of SUVECs. FB1 prevents cells from entering the S phase from the G1 phase by regulating the expression of the cell cycle-related genes cyclin B1, cyclin D1, cyclin E1, Cdc25c, and the cyclin-dependent kinase-4 (CDK-4). This results in an inhibition of cell proliferation. In addition, FB1 can also change the cell morphology, increase paracellular permeability, destroy tight junctions and the cytoskeleton, and reduce the expression of tight junction-related genes Claudin 1, Occludin, and ZO-1. This indicates that FB1 can cause cell barrier dysfunction of SUVECs and promote the weakening or even destruction of the connections between endothelial cells. In turn, this leads to increased blood vessel permeability and promotes exudation. Our findings suggest that FB1 induces toxicity in SUVECs by affecting cell proliferation and disrupting the barrier function.

MP81-18 EFFECTS OF SEX HORMONES ON CELL PROLIFERATION IN HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS

2017 ◽  
Vol 197 (4S) ◽  
Author(s):  
Yasumasa Miyazaki ◽  
Takeo Kosaka ◽  
Eiji Kikuchi ◽  
Akira Miyajima ◽  
Mototsugu Oya
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Sex Hormones ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Observations on Biological Effects of Carbon-13, Based on the Effects of 13C-Testosterone on Growth of Human Osteoblasts, Human Aortic Endothelial Cells, and Human Umbilical Vein Endothelial Cells in Vitro

2021 ◽  
Author(s):  
Mengqi Zhang ◽  
Wenning Yang ◽  
Xinchen Wu ◽  
Tengfei Zhang
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Isotope Effect ◽  
Umbilical Vein ◽  
Biological Effects ◽  
Bioactive Compound ◽  
Human Osteoblasts ◽  
Aortic Endothelial Cells ◽  
Umbilical Vein Endothelial Cells

Abstract Despite the increasing knowledge of biological isotope effect, comprehensive understanding of heavy isotope effect in the biological contexts has remained far less than expectation. The present study investigated the carbon isotope effect of 13C enriched testosterone on human cells. It was among the rare studies on carbon isotope effect of bioactive compound. Human osteoblasts, human aortic endothelial cells, and human umbilical vein endothelial cells were cultured in vitro and treated with testosterone and 13C enriched testosterone (13C/12C:6.7%). The impacts of physiological to pharmacological concentrations (10-10-10-5mol/L) of the bioactive compound were taken into account. The cell proliferation activities were measured using MTS assay. The levels of alkaline phosphatase and osteocalcin in osteoblasts were tested. Our results established that 13C enriched testosterone exhibited different biological effects from testosterone. At the concentrations of 10-10mol/L and 10-5mol/L, there were significant differences in prompting cell proliferation between testosterone and 13C enriched testosterone. At physiological concentrations, testosterone prompted proliferations of the three kinds of cells; whereas, 13C enriched testosterone did not prompt the cell proliferation, and its effects were not concentration dependent. At supraphysiological concentration (10-5mol/L), testosterone had the trend of inhibiting cell growth; whereas, 13C enriched testosterone had the trend of prompting cell growth. 13C enriched testosterone significantly enhanced osteocalcin secretion in human osteoblasts at supraphysiological concentration. These findings challenged the common view of growth retardation effect of heavy isotope, which imply that biological isotope effects are worthy of further study. The potential applications of 13C enriched compound were discussed.

scholarly journals Regulation of endothelial proliferation by the renin–angiotensin system in human umbilical vein endothelial cells

Reproduction ◽  
2008 ◽  
Vol 136 (1) ◽  
pp. 125-130 ◽  
Author(s):  
D Herr ◽  
M Rodewald ◽  
H M Fraser ◽  
G Hack ◽  
R Konrad ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Umbilical Vein ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Human Umbilical Vein ◽  
Renin Angiotensin ◽  
Umbilical Vein Endothelial Cells

This study was performed in order to evaluate the role of angiotensin II in physiological angiogenesis. Human umbilical vein endothelial cells (HUVEC) were stained for angiotensin II type 1 receptor (AGTR1) immunocytochemically and for gene expression of renin–angiotensin system (RAS) components. The regulation of the angiogenesis-associated genes vascular endothelial growth factor (VEGF) and angiopoietins (ANGPT1andANGPT2) were studied using quantitative RT-PCR. Furthermore, we examined the effect of angiotensin II on the proliferation of HUVEC using Ki-67 as well as BrdU immunocytochemistry and investigated whether the administration of the AGTR1 blocker candesartan or the VEGF antagonist FLT1-Fc could suppress the observed angiotensin II-dependent proangiogenic effect. AGTR1 was expressed in HUVEC and the administration of angiotensin II significantly increased the gene expression ofVEGFand decreased the gene expression ofANGPT1. Since the expression ofANGPT2was not affected significantly the ratio of ANGPT1/ANGPT2 was decreased. In addition, a significantly increased endothelial cell proliferation was observed after stimulation with angiotensin II, which was suppressed by the simultaneous administration of candesartan or the VEGF antagonist FLT1-Fc. These results indicate the potential capacity of angiotensin II in influencing angiogenesis by the regulation of angiogenesis-associated genes via AGTR1. Since VEGF blockade opposed the effect of angiotensin II on cell proliferation, it is hypothesised that VEGF mediates the angiotensin II-dependent effect in concert with the changes in angiopoietin expression. This is the first report of the RAS on the regulation of angiogenesis-associated genes in physiology.

The mononucleotide-dependent, nonantisense mechanism of action of phosphodiester and phosphorothioate oligonucleotides depends upon the activity of an ecto-5′-nucleotidase

Blood ◽  
2001 ◽  
Vol 98 (4) ◽  
pp. 995-1002 ◽  
Author(s):  
Maria Koziolkiewicz ◽  
Edyta Gendaszewska ◽  
Maria Maszewska ◽  
C. A. Stein ◽  
Wojciech J. Stec
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Enzymatic Degradation ◽  
Umbilical Vein ◽  
Cell Types ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Cytotoxic Effects ◽  
Specific Effects ◽  
Umbilical Vein Endothelial Cells

Many reports indicate different nonantisense yet sequence-specific effects of antisense phosphorothioate oligonucleotides. Products of enzymatic degradation of the oligonucleotides can also influence cell proliferation. The cytotoxic effects of deoxyribonucleoside-5′-phosphates (dNMPs) and their 5′-phosphorothioate analogs, deoxyribonucleoside-5′-monophosphorothioates (dNMPSs) on 4 human cell types (HeLa, HL-60, K-562, and endothelial cells) were examined, and the effects were correlated with the catabolism of these compounds. The results indicate that differences in cytotoxicity of dNMPs or dNMPSs in these cells depend upon different activity of an ecto-5′-nucleotidase. It has also been found that dNMPSs stimulate proliferation of human umbilical vein endothelial cells and HL-60 cells in a concentration-dependent manner. This stimulation might be caused by the binding of deoxynucleoside-5′-phosphorothioates to as-yet unidentified nucleotide receptor(s) at the cell surface.

scholarly journals A study of the effects of hydroxyapatite bioceramic extract on Ang/Tie2 system of umbilical vein endothelial cells

2021 ◽  
Vol 29 ◽  
pp. 531-538
Author(s):  
Xueyang Zhang ◽  
Yanyi Liu ◽  
Yuan Su ◽  
Xiaohui Fan ◽  
Fei Hu
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Umbilical Vein ◽  
Mrna Level ◽  
Cell Counting ◽  
Control Group ◽  
Real Time Quantitative Pcr ◽  
Student’S T ◽  
Umbilical Vein Endothelial Cells ◽  
Student’S T Test

OBJECTIVE: We aimed to investigate the effects of hydroxyapatite bioceramic extract on Ang/Tie2 system and cell proliferation of umbilical vein endothelial cells. METHODS: Human umbilical vein endothelial cells (HUVECs) were used in this research. There are two induvial groups, control group and hydroxyapatite bioceramics extract treatment group. Cell Counting Kit-8 (CCK-8) was used to evaluate cell proliferation. Western blot and real time quantitative PCR (Q-PCR) were used to evaluate the protein and mRNA expression levels of Ang1, Ang2 and Tie2 in Ang/Tie2 system, respectively. All the results were statistically analyzed by Spss19.0. All data were presented as mean ± standard error of mean (SEM). Student’s t-test was performed to determine the differences among grouped data. RESULTS: Hydroxyapatite bioceramics extract showed no effect on the cell morphology and cell proliferation of HUVECs. Interestingly, we found that both Ang2 and Tie2 protein and mRNA level were markedly increased by hydroxyapatite bioceramics extract. CONCLUSIONS: Hydroxyapatite bioceramic extract showed no cytotoxicity to HUVECs, and might regulate vascular remodeling by mediating Ang/Tie2 system.

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