scholarly journals Organizational behavior of human umbilical vein endothelial cells.

1982 ◽  
Vol 94 (3) ◽  
pp. 511-520 ◽  
Author(s):  
T Maciag ◽  
J Kadish ◽  
L Wilkins ◽  
M B Stemerman ◽  
R Weinstein
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Organizational Behavior ◽  
Umbilical Vein ◽  
Ultrastructural Level ◽  
Tube Formation ◽  
Culture Conditions ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Culture conditions that favor rapid multiplication of human umbilical vein endothelial cells (HUV-EC) also support long-term serial propagation of the cells. This is routinely achieved when HUV-EC are grown in Medium 199 (M-199) supplemented with fetal bovine serum (FBS) and endothelial cell growth factor (ECGF), on a human fibronectin (HFN) matrix. The HUV-EC can shift from a proliferative to an organized state when the in vitro conditions are changed from those favoring low density proliferation to those supporting high density survival. When ECGF and HFN are omitted, cultures fail to achieve confluence beyond the first or second passage: the preconfluent cultures organize into tubular structures after 4-6 wk. Some tubes become grossly visible and float in the culture medium, remaining tethered to the plastic dish at either end of the tube. On an ultrastructural level, the tubes consist of cells, held together by junctional complexes, arranged so as to form a lumen. The smallest lumens are formed by one cell folding over to form a junction with itself. The cells contain Weibel-Palade bodies and factor VIII-related antigen. The lumens contain granular, fibrillar and amorphous debris. Predigesting the HFN matrix with trypsin (10 min, 37 degrees C) or plasmin significantly accelerates tube formation. Thrombin and plasminogen activator had no apparent effect. Disruption of the largest tubes with trypsin/EDTA permits the cells to revert to a proliferative state if plated on HFN, in M-199, FBS, and ECGF. These observations indicate that culture conditions that do not favor proliferation permit attainment of a state of nonterminal differentiation (organization) by the endothelial cell. Furthermore, proteolytic modification of the HFN matrix may play an important role in endothelial organization.

Abstract 101: MiR-4260 Promotes the Proliferation, Migration, and Tube Formation of Human Umbilical Vein Endothelial Cells

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Qi Sun ◽  
Dongcao Lv ◽  
Qiulian Zhou ◽  
Yihua Bei ◽  
Junjie Xiao
Keyword(s):  
Endothelial Cells ◽  
Target Genes ◽  
Cell Function ◽  
Umbilical Vein ◽  
Tube Formation ◽  
Endothelial Cell Function ◽  
Human Umbilical Vein ◽  
And Migration ◽  
Umbilical Vein Endothelial Cells

MicroRNAs (miRNAs, miRs), endogenous small non-coding RNA, have been shown to act as essential regulators in angiogenesis which plays important roles in improving blood flow and cardiac function following myocardial infarction. The current study investigated the potential of miR-4260 in endothelial cell function and angiogenesis using human umbilical vein endothelial cells (HUVEC). Our data demonstrated that overexpression of miR-4260 was associated with increased proliferation and migration of HUVEC using EdU incorporation assay (17.25%±1.31 vs 25.78%±1.24 in nc-mimics vs miR-4260 mimics, respectively) and wound healing assay, respectively. While downregulation of miR-4260 inhibited the proliferation (17.90%±1.37 vs 10.66%±1.41 in nc-inhibitor vs miR-4260 inhibitor, respectively) and migration of HUVEC. Furthermore, we found that miR-4260 mimics increased (129.75±3.68 vs 147±3.13 in nc-mimics vs miR-4260 mimics, respectively), while miR-4260 inhibitor decreased the tube formation of HUVECs in vitro (123.25±2.17 vs 92±4.45 in nc-inhibitor vs miR-4260 inhibitor expression, respectively). Our data indicate that miR-4260 contributes to the proliferation, migration and tube formation of endothelial cells, and might be essential regulators for angiogenesis. Further study is needed to investigate the underlying mechanism that mediates the role of miR-4260 in angiogenesis by identifying its putative downstream target genes.

scholarly journals Immunosuppressive nano-therapeutic micelles downregulate endothelial cell inflammation and immunogenicity

RSC Advances ◽  
2015 ◽  
Vol 5 (54) ◽  
pp. 43552-43562 ◽  
Author(s):  
Satish N. Nadig ◽  
Suraj K. Dixit ◽  
Natalie Levey ◽  
Scott Esckilsen ◽  
Kayla Miller ◽  
...  
Keyword(s):  
Immune Response ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Perfusion Solution ◽  
Umbilical Vein Endothelial Cells

Targeted micelles containing rapamycin (TRaM) suppressed the immune response of IL-8 in oxidatively stressed human umbilical vein endothelial cellsin vitro(a) and accumulated in aorta grafts for transplantation after 6 hours in cold perfusion solution (b).

scholarly journals Long-Zhi Decoction Medicated Serum Promotes Angiogenesis in Human Umbilical Vein Endothelial Cells Based on Autophagy

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Quan He ◽  
Qihua Liu ◽  
Yongbin Chen ◽  
Jiaquan Meng ◽  
Ling Zou
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Vascular Diseases ◽  
The Elderly ◽  
Tube Formation ◽  
Beclin 1 ◽  
Effective Response ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

Ischemic stroke (IS) is a fatal subtype of stroke that lacks effective treatments. Angiogenesis following IS is an effective response that mediates brain recovery and repair. Our previous study demonstrated that long-zhi decoction (LZD), a Chinese herbal formula, promoted angiogenesis in rats of IS model. To further investigate the association between the proangiogenic mechanism of an LZD-medicated serum and cellular autophagy, we evaluated its promotional effect on angiogenesis in human umbilical vein endothelial cells (HUVECs) in vitro. We used HUVECs subjected to H2O2 to induce injury and observed the effects of the LZD-medicated serum treatment. Cell-based assays included proliferation, migration, and tube formation. To assess the extent of autophagy, transmission electron microscopy was used to measure the number of autophagosomes. Immunofluorescence and Western blotting were performed to evaluate the autophagy-related protein of LC3-II and Beclin-1. The LZD-medicated serum promoted proliferation, migration, and tube formation in HUVECs. The LZD-medicated serum also increased the autophagosomes and the autophagic protein expressions of LC3-II and Beclin-1. The proangiogenic and autophagic activity of LZD provides new cogitations to its clinical application and may lead to potential drug development for treating various vascular diseases, especially in the elderly, in the future.

scholarly journals Interleukin-1βExpression Is Required for Lysophosphatidic Acid-Induced Lymphangiogenesis in Human Umbilical Vein Endothelial Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Chih-Hsin Lin ◽  
JenHer Lu ◽  
Hsinyu Lee
Keyword(s):  
Endothelial Cells ◽  
Lysophosphatidic Acid ◽  
Umbilical Vein ◽  
Tube Formation ◽  
Lipid Mediator ◽  
Vascular Endothelial ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells ◽  
Endothelial Growth Factor

Lysophosphatidic acid (LPA) is a lipid mediator which binds to G-protein-coupled receptors and regulates various cellular responses, including inflammation of endothelial cells. Interleukin- (IL-) 1β, a proinflammatory cytokine, is elevated upon LPA treatment in human umbilical vein endothelial cells (HUVECs). Previous studies indicated that LPA upregulates vascular endothelial growth factor- (VEGF-) C and lymphatic marker expressions in HUVECs. However, the relationships between LPA-induced VEGF-C and IL-1βexpressions are not clear. In this paper, we demonstrated that, in the presence of AF12198, an inhibitor of the IL-1 receptor abolished LPA-induced VEGF-C and lymphatic marker expressions in HUVECs. Furthermore, LPA-inducedin vitrotube formation of HUVECs was also suppressed by pretreatment with AF12198. Our results suggest that LPA-stimulated lymphangiogenesis in HUVECs is mediated through IL-1β-induced VEGF-C expression.

scholarly journals Comparative analysis of the effects of opioids in angiogenesis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tao Feng ◽  
Si Zeng ◽  
Jie Ding ◽  
Gong Chen ◽  
Bin Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Tube Formation ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Apoptotic Effect ◽  
Toxicity Of Drugs ◽  
Umbilical Vein Endothelial Cells

Abstract Background Angiogenesis, the formation of blood vessel from pre-existing ones, plays an important role in many pathophysiological diseases, such as cancer. Opioids are often used in clinic for the management of chronic pain in cancer patients at terminal phases. Here, we investigated and compared the effects and mechanisms of four opioids on angiogenesis. Methods We performed angiogenesis assays on human umbilical vein endothelial cells (HUVEC) that represent an in vitro model to assess the toxicity of drugs to endothelium. Results Morphine and oxycodone at 0.1 μM to 100 μM dose-dependently increased endothelial cell tube formation and proliferation. We observed the same in endothelial cells exposed to fentanyl at 0.1 μM to 10 μM but there was a gradual loss of stimulation by fentanyl at 100 μM and 1000 μM. Morphine and fentanyl reduced endothelial cell apoptosis-induced by serum withdrawal whereas oxycodone did not display anti-apoptotic effect, via decreasing Bax level. Oxycodone at the same concentrations was less potent than morphine and fentanyl. Different from other three opioids, codeine at all tested concentrations did not affect endothelial cell tube formation, proliferation and survival. Mechanism studies demonstrated that opioids acted on endothelial cells via μ-opioid receptor-independent pathway. Although we observed the increased phosphorylation of mitogen-activated protein kinase (MAPK) in cells exposed to morphine, fentanyl and oxycodone, the rescue studies demonstrated that the stimulatory effects of morphine but not fentanyl nor oxycodone were reversed by a specific MAPK inhibitor. Conclusion Our work demonstrates the differential effects and mechanisms of opioids on angiogenesis.

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