Sirtuin 6 (SIRT6) Content and Hypoxia‐Inducible Factor 1‐Alpha (HIF‐1α) Expression in Human Umbilical Vein Endothelial Cells (HUVECs) in Response to Cyanidin‐3‐O‐ β‐glucoside (C3G): Pregnancy Complicated by Diabetes (PCD) vs. Normoglycemic Pregnancy (NP)

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Dariusz Szukiewicz ◽  
Mateusz Watroba ◽  
Grzegorz Szewczyk ◽  
Piotr Wojdasiewicz
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Hypoxia Inducible Factor ◽  
Human Umbilical Vein ◽  
Hypoxia Inducible Factor 1 ◽  
Umbilical Vein Endothelial Cells

Pulsed high oxygen induces a hypoxic-like response in human umbilical endothelial cells and in humans

2012 ◽  
Vol 113 (11) ◽  
pp. 1684-1689 ◽  
Author(s):  
F. Cimino ◽  
C. Balestra ◽  
P. Germonpré ◽  
D. De Bels ◽  
F. Tillmans ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Hypoxia Inducible Factor ◽  
Activity Level ◽  
Gene Expressions ◽  
Functional Level ◽  
Normobaric Oxygen ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

It has been proposed that relative changes of oxygen availability, rather than steady-state hypoxic or hyperoxic conditions, play an important role in hypoxia-inducible factor (HIF) transcriptional effects. According to this hypothesis describing the “normobaric oxygen paradox”, normoxia following a hyperoxic event is sensed by tissues as an oxygen shortage, upregulating HIF-1 activity. With the aim of confirming, at cellular and at functional level, that normoxia following a hyperoxic event is “interpreted” as a hypoxic event, we report a combination of experiments addressing the effects of an intermittent increase of oxygen concentration on HIF-1 levels and the activity level of specific oxygen-modulated proteins in cultured human umbilical vein endothelial cells and the effects of hemoglobin levels after intermittent breathing of normobaric high (100%) and low (15%) oxygen in vivo in humans. Our experiments confirm that, during recovery after hyperoxia, an increase of HIF expression occurs in human umbilical vein endothelial cells, associated with an increase of matrix metalloproteinases activity. These data suggest that endothelial cells “interpret” the return to normoxia after hyperoxia as a hypoxic stimulus. At functional level, our data show that breathing both 15 and 100% oxygen 30 min every other day for a period of 10 days induces an increase of hemoglobin levels in humans. This effect was enhanced after the cessation of the oxygen breathing. These results indicate that a sudden decrease in tissue oxygen tension after hyperoxia may act as a trigger for erythropoietin synthesis, thus corroborating the hypothesis that “relative” hypoxia is a potent stimulator of HIF-mediated gene expressions.

PGE1analog alprostadil induces VEGF and eNOS expression in endothelial cells

2005 ◽  
Vol 289 (5) ◽  
pp. H2066-H2072 ◽  
Author(s):  
Dominik G. Haider ◽  
Robert A. Bucek ◽  
Aura G. Giurgea ◽  
Gerald Maurer ◽  
Helmut Glogar ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Hypoxia Inducible Factor ◽  
Disease Process ◽  
Hypoxia Inducible Factor 1 ◽  
Hypoxic Conditions ◽  
Umbilical Vein Endothelial Cells ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Endothelial nitric oxide synthase (eNOS), VEGF, and hypoxia-inducible factor 1-α (HIF-1α) are important regulators of endothelial function, which plays a role in the pathophysiology of heart failure (HF). PGE1analog treatment in patients with HF elicits beneficial hemodynamic effects, but the precise mechanisms have not been investigated. We have investigated the effects of the PGE1analog alprostadil on eNOS, VEGF, and HIF-1α expression in human umbilical vein endothelial cells (HUVEC) using RT-PCR and immunoblotting under normoxic and hypoxic conditions. In addition, we studied protein expression by immunohistochemical staining in explanted hearts from patients with end-stage HF, treated or untreated with systemic alprostadil. Alprostadil causes an upregulation of eNOS and VEGF protein and mRNA expression in HUVEC and decreases HIF-1α. Hypoxia potently increased eNOS, VEGF, and HIF-1α synthesis. The alprostadil-induced upregulation of eNOS and VEGF was prevented by inhibition of MAPKs with PD-98056 or U-0126. Consistently, the expression of eNOS and VEGF was increased, and HIF-1α was reduced in failing hearts treated with alprostadil. The potent effects of alprostadil on endothelial VEGF and eNOS synthesis may be useful for patients with HF where endothelial dysfunction is involved in the disease process.

Studies of the Factor Xa-Dependent Inhibitor of Factor VIIa/Tissue Factor (Extrinsic Pathway Inhibitor) from Cell Supernates of Cultured Human Umbilical Vein Endothelial Cells

1989 ◽  
Vol 61 (01) ◽  
pp. 101-105 ◽  
Author(s):  
Bonnie J Warn-Cramer ◽  
Fanny E Almus ◽  
Samuel I Rapaport
Keyword(s):  
Molecular Weight ◽  
Endothelial Cells ◽  
Tissue Factor ◽  
Phorbol Ester ◽  
Umbilical Vein ◽  
Primary Cultures ◽  
Factor Xa ◽  
Extrinsic Pathway ◽  
Human Umbilical Vein ◽  
Umbilical Vein Endothelial Cells

SummaryCultured human umbilical vein endothelial cells (HUVEC) have been reported to produce extrinsic pathway inhibitor (EPI), the factor Xa-dependent inhibitor of factor VHa/tissue factor (TF). We examined the release of this inhibitor from HUVEC as a function of their growth state and in response to the induction of endothelial cell TF activity. HUVEC constitutively produced significant amounts of EPI at all stages of their growth in culture including the post-confluent state. Rate of release varied over a 3-fold range for primary cultures from 12 different batches of pooled umbilical cord cells. Constitutive EPI release was unaltered during a 6 hour period of induction of TF activity with thrombin or phorbol ester but slowed during longer incubation of the cells with phorbol ester. Whereas plasma contains two molecular weight forms of EPI, only the higher of these two molecular weight forms was demonstrable by Western analysis of HUVEC supernatants with 125I-factor Xa as the ligand.

Partial Characterization of a Fibrinolytic Inhibitor Produced by Cultured Endothelial Cells Derived from Human Umbilical Vein

1982 ◽  
Vol 47 (02) ◽  
pp. 128-131 ◽  
Author(s):  
F Esnard ◽  
E Dupuy ◽  
A M Dosne ◽  
E Bodevin
Keyword(s):  
Endothelial Cells ◽  
Primary Culture ◽  
Ammonium Sulphate ◽  
Concanavalin A ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
Preliminary Characterization ◽  
Umbilical Vein Endothelial Cells ◽  
Ammonium Sulphate Saturation

SummaryA preliminary characterization of a fibrinolytic inhibitor released by human umbilical vein endothelial cells in primary culture is reported. This molecule of Mr comprised between 2 × 105 and 106 and of μ2 mobility precipitates at 43% ammonium sulphate saturation and is totally adsorbed on Concanavalin A Sepharose 4 B. A possible relationship with a macroglobulins is discussed.

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