Inhibition of angiogenic key features: the Amaryllidaceae alkaloid narciclasine diminishes proliferation, migration, tube formation and sprouting of human endothelial cells

2017 ◽  
Author(s):  
J Bräutigam ◽  
L Nguyen Dieu ◽  
E Heiss ◽  
I Bischoff ◽  
R Fürst
Keyword(s):  
Endothelial Cells ◽  
Tube Formation ◽  
Human Endothelial Cells ◽  
Key Features

scholarly journals Constitutive expression of E-and P-selectin cognate ligands in human endothelial cells

1998 ◽  
Vol 7 (3) ◽  
pp. 211-215
Author(s):  
C. Palma ◽  
D. Bellarosa ◽  
F. Nardelli ◽  
G. Mannori ◽  
S. Manzini
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Blood Cells ◽  
Constitutive Expression ◽  
Tube Formation ◽  
Human Endothelial Cells ◽  
Selectin Ligands ◽  
Ligand Expression ◽  
Huvec Cells ◽  
Promote Cell Adhesion

On human endothelial cells from umbilical cord (HUVEC) are present, in addition to E-and P-selectins, their cognate ligands. Differently from selectins, the ligand expression is constitutive and not modulated by interleukin-1β . Such ligands appear to be different from the ones present in promyelocytic cells in order to promote cell adhesion to immobilized selectins. The expression of selectin-ligands on HUVEC cells suggest that selectins can participate in endothelial signalling besides their role as adhesion molecules for circulating blood cells. However, despite their role in chemotaxis, selectins do not contribute to HUVEC tube formation in Matrigel.

scholarly journals IL-6 trans-Signaling Impairs Sprouting Angiogenesis by Inhibiting Migration, Proliferation and Tube Formation of Human Endothelial Cells

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1414
Author(s):  
Mulugeta M Zegeye ◽  
Blanka Andersson ◽  
Allan Sirsjö ◽  
Liza U Ljungberg
Keyword(s):  
Endothelial Cells ◽  
Molecular Mechanisms ◽  
Tube Formation ◽  
Angiogenic Factors ◽  
Vascular Endothelial ◽  
Human Endothelial Cells ◽  
Angiogenic Response ◽  
Sprouting Angiogenesis ◽  
Endothelial Growth Factor ◽  
Shed Light

Sprouting angiogenesis is the formation of new capillaries from existing vessels in response to tissue hypoxia due to growth/development, repair/healing, and also chronic inflammation. In this study, we aimed to elucidate the effect of IL-6, a pleiotropic cytokine with both pro-inflammatory and anti-inflammatory functions, in regulating the sprouting angiogenic response of endothelial cells (ECs). We found that activation of IL-6 trans-signaling inhibited the migration, proliferation, and tube formation ability of ECs. In addition, inhibition of the autocrine IL-6 classic-signaling by depleting endogenous IL-6 from ECs impaired their tube formation ability. At the molecular level, we found that IL-6 trans-signaling in ECs upregulated established endogenous anti-angiogenic factors such as CXCL10 and SERPINF1 while at the same time downregulated known endogenous pro-angiogenic factors such as cKIT and CXCL8. Furthermore, prior activation of ECs by IL-6 trans-signaling alters their response to vascular endothelial growth factor-A (VEGF-A), causing an increased p38, but decreased Erk1/2 phosphorylation. Collectively, our data demonstrated the dual facets of IL-6 in regulating the sprouting angiogenic function of ECs. In addition, we shed light on molecular mechanisms behind the IL-6 trans-signaling mediated impairment of endothelial sprouting angiogenic response.

scholarly journals Toxic Damage Increases Angiogenesis and Metastasis in Fibrotic Livers via PECAM-1

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Esther Raskopf ◽  
Maria Angeles Gonzalez Carmona ◽  
Christina Jay Van Cayzeele ◽  
Christian Strassburg ◽  
Tilman Sauerbruch ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Liver Damage ◽  
Tube Formation ◽  
Ethanol Exposure ◽  
Human Endothelial Cells ◽  
Cell Functions ◽  
Promising Tool ◽  
Toxic Damage

Excessive ethanol consumption is one of the main causes of liver fibrosis. However, direct effects of ethanol exposure on endothelial cells and their contribution to fibrogenesis and metastasis were not investigated. Therefore we analysed whether ethanol directly affects endothelial cells and if this plays a role during fibrogenesis and metastasis in the liver. Murine and human endothelial cells were exposed to ethanol for up to 72 hours.In vitro, effects on VEGF, HIF-1alpha, PECAM-1, and endothelial cell functions were analysed.In vivo, effects of continuous liver damage on blood vessel formation and metastasis were analysed by PECAM-1 immunohistochemistry. Ethanol increased HIF-1alpha and VEGF levels in murine and human endothelial cells. This resulted in enhanced intracellular signal transduction, and PECAM-1 expression as well as tube formation and wound healing.In vivo, toxic liver damage increased angiogenesis during fibrogenesis. Metastasis was also enhanced in fibrotic livers and located to PECAM-1 positive blood vessels compared to nonfibrotic mice. In conclusion, ethanol had strong effects on endothelial cells, which—at least in part—led to a profibrotic and prometastatic environment mediated by PECAM-1. Blockade of increased PECAM-1 expression could be a promising tool to inhibit fibrogenesis and metastasis in the liver.

Depletion of the novel protein PHACTR-1 from human endothelial cells abolishes tube formation and induces cell death receptor apoptosis

Biochimie ◽  
2011 ◽  
Vol 93 (10) ◽  
pp. 1668-1675 ◽  
Author(s):  
Rafika Jarray ◽  
Barbara Allain ◽  
Lucia Borriello ◽  
Denis Biard ◽  
Ali Loukaci ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Death ◽  
Death Receptor ◽  
Tube Formation ◽  
The Novel ◽  
Human Endothelial Cells ◽  
Cell Death Receptor ◽  
Novel Protein

scholarly journals Impact of DICER1 and DROSHA on the Angiogenic Capacity of Human Endothelial Cells

2021 ◽  
Vol 22 (18) ◽  
pp. 9855
Author(s):  
Heike Braun ◽  
Michael Hauke ◽  
Anne Ripperger ◽  
Christian Ihling ◽  
Matthew Fuszard ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Umbilical Vein ◽  
Expression Profiles ◽  
Angiogenesis Inhibitor ◽  
Tube Formation ◽  
Brdu Incorporation ◽  
Mirna Biogenesis ◽  
Human Endothelial Cells

RNAi-mediated knockdown of DICER1 and DROSHA, enzymes critically involved in miRNA biogenesis, has been postulated to affect the homeostasis and the angiogenic capacity of human endothelial cells. To re-evaluate this issue, we reduced the expression of DICER1 or DROSHA by RNAi-mediated knockdown and subsequently investigated the effect of these interventions on the angiogenic capacity of human umbilical vein endothelial cells (HUVEC) in vitro (proliferation, migration, tube formation, endothelial cell spheroid sprouting) and in a HUVEC xenograft assay in immune incompetent NSGTM mice in vivo. In contrast to previous reports, neither knockdown of DICER1 nor knockdown of DROSHA profoundly affected migration or tube formation of HUVEC or the angiogenic capacity of HUVEC in vivo. Furthermore, knockdown of DICER1 and the combined knockdown of DICER1 and DROSHA tended to increase VEGF-induced BrdU incorporation and induced angiogenic sprouting from HUVEC spheroids. Consistent with these observations, global proteomic analyses showed that knockdown of DICER1 or DROSHA only moderately altered HUVEC protein expression profiles but additively reduced, for example, expression of the angiogenesis inhibitor thrombospondin-1. In conclusion, global reduction of miRNA biogenesis by knockdown of DICER1 or DROSHA does not inhibit the angiogenic capacity of HUVEC. Further studies are therefore needed to elucidate the influence of these enzymes in the context of human endothelial cell-related angiogenesis.

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