scholarly journals VEGF-C/VEGFR-3/iNOS Signaling in Osteosarcoma MG63 Cells Mediates Their Stimulatory Effects on Human Umbilical Vein Endothelial Cell Proliferation

2021 ◽  
Vol 0 (0) ◽  
pp. 1
Author(s):  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Endothelial Cell Proliferation ◽  
Human Umbilical Vein ◽  
Mg63 Cells

Platelets induce human umbilical vein endothelial cell proliferation through P-selectin

Life Sciences ◽  
2000 ◽  
Vol 66 (19) ◽  
pp. 1817-1826 ◽  
Author(s):  
Sisi Marcondes ◽  
Monique Lafay ◽  
Brigitte Brohard-Bohn ◽  
Gilberto De Nucci ◽  
Francine Rendu
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Endothelial Cell Proliferation ◽  
Human Umbilical Vein

scholarly journals Phyllanthus emblicaL. Enhances Human Umbilical Vein Endothelial Wound Healing and Sprouting

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Linda Chularojmontri ◽  
Maneewan Suwatronnakorn ◽  
Suvara K. Wattanapitayakul
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Endothelial Cell Proliferation ◽  
Total Phenolic ◽  
No Production ◽  
Impaired Wound Healing ◽  
Human Umbilical Vein ◽  
Increased Risk

Endothelial dysfunction is the hallmark of impaired wound healing and increased risk of cardiovascular disease. Antioxidants from natural sources decrease oxidative stress and protect against cellular damage caused by reactive oxygen species (ROS). In this study, we examined the antioxidant constituents and capacity ofPhyllanthus emblicaL. (PE) fruit in freeze-dried power form. The pharmacological properties of PE were investigated using human umbilical vein endothelial cells (HUVECs) in the aspects of endothelial cell proliferation, nitric oxide (NO) production, wound healing, cell migration,in vitroangiogenesis, and VEGF gene expression. The ASC content of PE was 1.574% + 0.046% (w/w) as determined by HPLC and the total phenolic content was 36.1% ± 0.7% gallic acid equivalent when measured by Folin-Ciocalteu assay. The FRAP assay revealed a relatively high antioxidant capacity at 3,643 + 192.5 µmole/mg. PE at 0.1 to 10 µg/mL did not significantly influence endothelial cell proliferation, but at higher concentrations PE decreased cell survival to 62%. PE significantly promoted NO production, endothelial wound closure, endothelial sprouting, and VEGF mRNA expression. Therefore, PE is a candidate for antioxidant supplement that promotes endothelial function and restores wound healing competency.

Inhibition of Human Umbilical Vein Endothelial Cell Proliferation by the CXC Chemokine, Platelet Factor 4 (PF4), Is Associated With Impaired Downregulation of p21Cip1/WAF1

Blood ◽  
1999 ◽  
Vol 93 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Grazia Gentilini ◽  
Nancy E. Kirschbaum ◽  
James A. Augustine ◽  
Richard H. Aster ◽  
Gian Paolo Visentin
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Cyclin E ◽  
Endothelial Cell Proliferation ◽  
Cyclin Dependent Kinase ◽  
Platelet Factor ◽  
Human Umbilical Vein ◽  
Cdk2 Activity

Human PF4 is a heparin-binding chemokine known to be capable of inhibiting endothelial cell proliferation and angiogenesis. To explore the biological mechanisms responsible for this action, we investigated the effect of PF4 on epidermal growth factor (EGF)-stimulated human umbilical vein endothelial cells (HUVEC), a model system in which stimulation is essentially independent of interaction with cell-surface glycosaminoglycans. Based on previous findings that PF4 blocks endothelial cell cycle entry and progression into S phase, we studied the molecular mechanism(s) of PF4 interference with cell cycle machinery. PF4 treatment of EGF-stimulated HUVEC caused a decrease in cyclin E–cyclin-dependent kinase 2 (cdk2) activity with resulting attenuation of retinoblastoma protein phosphorylation. PF4-dependent downregulation of cyclin E-cdk2 activity was associated with increased binding of the cyclin-dependent kinase inhibitor, p21Cip1/WAF1, to the cyclin E-cdk2 complex. Analysis of total cellular p21Cip1/WAF1 showed that in the presence of PF4, p21Cip1/WAF1 levels were sustained at time points when p21Cip1/WAF1 was no longer detectable in cells stimulated by EGF in the absence of PF4. These findings indicate that PF4 inhibition of HUVEC proliferation in response to EGF is associated with impaired downregulation of p21Cip1/WAF1 and provide the first evidence for interference with cell cycle mechanisms by a chemokine.

Efficacy of dextran and peptide-everolimus bi-directional stent

2019 ◽  
Vol 33 (9) ◽  
pp. 1232-1241 ◽  
Author(s):  
So Youn Lee ◽  
Eun Jae Jang ◽  
In-Ho Bae ◽  
Dae Sung Park ◽  
Doo Sun Sim ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Fluorescein Isothiocyanate ◽  
Surface Shape ◽  
University Hospital ◽  
Endothelial Cell Proliferation ◽  
Nuclear Staining ◽  
Human Umbilical Vein

Everolimus inhibits stent restenosis and the WKYMV (fluorescein isothiocyanate) peptide promotes endothelial homing. Dextran is a natural polymer that is widely used as a pharmaceutical agent. The purpose of this study was to develop a double-drug-coated stent using a bidirectional coating system and to examine the surface shape with in vitro experiments. Stent length was 16 mm and strut thickness was 70 µm (Chonnam National University Hospital Tiger stent). Optical and scanning electron microscopy showed good coating without cracks or bubbles. Fluorescein isothiocyanate-peptide was dip-coated on the lumen and the abluminal surface was coated with everolimus and dextran. Stents were coated with dextran, everolimus, or everolimus–dextran. The radial force and flexibility were measured to determine the mechanical properties. Contact angle testing was performed in all groups. Dextran and peptide as hydrophilic substances and everolimus as a hydrophobic substance were each coated on cover glasses (cobalt–chromium). A10 and human umbilical vein endothelial cells were used in the experiments. Water and dimethyl sulfoxide served as a control, and three drug groups were tested: peptide–everolimus, everolimus–dextran, and peptide–everolimus–dextran. Immunocytochemistry was performed to assess cell adhesion. Light intensity was plotted according to the average on nuclear staining. Experiments were conducted using 5-bromo-2′-deoxyuridine to investigate A10 and human umbilical vein endothelial cell proliferation. Cell adhesion and proliferation of peptide–everolimus–dextran were inhibited at A10, and human umbilical vein endothelial cell was found to proliferate with cell adhesion. On conclusion, dextran and peptide–everolimus bidirectional stent is effective in re-endothelialization and inhibition of cell proliferation.

Inhibition of Human Umbilical Vein Endothelial Cell Proliferation by the CXC Chemokine, Platelet Factor 4 (PF4), Is Associated With Impaired Downregulation of p21Cip1/WAF1

Blood ◽  
1999 ◽  
Vol 93 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Grazia Gentilini ◽  
Nancy E. Kirschbaum ◽  
James A. Augustine ◽  
Richard H. Aster ◽  
Gian Paolo Visentin
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Cyclin E ◽  
Endothelial Cell Proliferation ◽  
Cyclin Dependent Kinase ◽  
Platelet Factor ◽  
Human Umbilical Vein ◽  
Cdk2 Activity

Abstract Human PF4 is a heparin-binding chemokine known to be capable of inhibiting endothelial cell proliferation and angiogenesis. To explore the biological mechanisms responsible for this action, we investigated the effect of PF4 on epidermal growth factor (EGF)-stimulated human umbilical vein endothelial cells (HUVEC), a model system in which stimulation is essentially independent of interaction with cell-surface glycosaminoglycans. Based on previous findings that PF4 blocks endothelial cell cycle entry and progression into S phase, we studied the molecular mechanism(s) of PF4 interference with cell cycle machinery. PF4 treatment of EGF-stimulated HUVEC caused a decrease in cyclin E–cyclin-dependent kinase 2 (cdk2) activity with resulting attenuation of retinoblastoma protein phosphorylation. PF4-dependent downregulation of cyclin E-cdk2 activity was associated with increased binding of the cyclin-dependent kinase inhibitor, p21Cip1/WAF1, to the cyclin E-cdk2 complex. Analysis of total cellular p21Cip1/WAF1 showed that in the presence of PF4, p21Cip1/WAF1 levels were sustained at time points when p21Cip1/WAF1 was no longer detectable in cells stimulated by EGF in the absence of PF4. These findings indicate that PF4 inhibition of HUVEC proliferation in response to EGF is associated with impaired downregulation of p21Cip1/WAF1 and provide the first evidence for interference with cell cycle mechanisms by a chemokine.

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