Reactions of Human Endothelial Cell Cultures Exposed to Adrenalin Concentrations

1975 ◽  
Author(s):  
Payling H. Wright ◽  
M. Evans
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Cultures ◽  
Vascular Endothelium ◽  
Human Endothelial Cell ◽  
Cultural Conditions ◽  
Endothelial Cell Cultures

Cultures of vascular endothelium obtained from fresh human umbilical veins and grown in vitro in fortified 199 medium for several days have been subjected to differing concentrations of adrenalin for various times. Their reactions to the drug, as seen microscopically, were recorded photographically. The viability of endothelial cells under these cultural conditions gives a measure of the maximal exposure to adrenalin which they are able not only to survive, but also to multiply. Their capacity to mitose was studied autor adiographically.The significance of the findings will be discussed with reference to atherogenesis and particularly the possible link with infection and in “stress”.

scholarly journals The Interaction of the Platelet and von Willebrand Factor

1977 ◽  
Author(s):  
D.N. Fass ◽  
F. Booyse ◽  
J.C. Lewis ◽  
E. J. W. Bowie
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Cultures ◽  
Von Willebrand Factor ◽  
Sandwich Technique ◽  
Aortic Endothelial Cells ◽  
Confluent Culture ◽  
Endothelial Cell Cultures ◽  
Von Willebrand ◽  
Willebrand Factor

A culture of pig aortic endothelial cells was used for experiments to investigate the interaction between the platelet and von Willebrand factor. An antibody was raised in rabbits to purified porcine von Willebrand factor. A semi-confluent culture of pig endothelial cells was stained immunofluorescently by the sandwich technique using anti-Willebrand factor IgG. An extensive extracellular meshwork of microfilaments was revealed. In endothelial cell cultures from von Willebrand pigs, no immunoreactive microfilaments were found. Immunoelectronmicro-scopy with peroxidase linked antibody has been used to identify similar filaments in normal pig endothelial cells. Washed platelets were shown to adhere to semiconfluent or damaged normal endothelial cell cultures. If the cultures had been previously incubated with anti-Willebrand factor IgG, the washed platelets did not adhere. There was no adherence of platelets when they were added to semiconfluent or damaged von Willebrand endothelial cells.

Induction of endothelial proliferation and angiogenesis through activating the ERK1/2/EGF pathway mediate by CXC chemokine receptor 2 by chemokine (C-X-C motif) ligand 1.

2013 ◽  
Vol 31 (6_suppl) ◽  
pp. 138-138 ◽  
Author(s):  
Makito Miyake ◽  
Steve Goodison ◽  
Evan Gomes ◽  
Wasia Rizwani ◽  
Shanti Ross ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Chemokine Receptor ◽  
Cellular Proliferation ◽  
Human Endothelial Cell ◽  
Endothelial Cell Proliferation ◽  
Cxc Chemokine ◽  
Inhibition Of Angiogenesis

138 Background: Endothelial cell growth and proliferation are critical for tumoral angiogenesis. We report here that blockade of Chemokine (C-X-C motif) ligand 1 (CXCL1) results in reduction of human endothelial cell proliferation and its ability to induce angiogenesis. Methods: Two human endothelial cell lines, HUVEC and HDMEC, were used in the in vitro assays. Proliferation assay and matrigel tube formation assay were performed to test the inhibitory effect of anti-CXCL antibody on the activity of endothelial cells in vitro. Matrigel plug assay in nude mice was performed to test the in vivo angiogenic activity of CXCL1. Results: CXCL1 interacts with its receptor CXC chemokine Receptor 2 and induces endothelial cell proliferation, whereas blockade of CXCL1 is associated with reduction in cellular proliferation through a decrease in levels of cyclin D and cdk4 and inhibition of angiogenesis through EGF and ERK 1/2. Targeting CXCL1 inhibits neoangiogenesis but has no effect on disrupting established vasculature. Furthermore targeting CXCL1 is associated with reduction in migration of human endothelial cells in an in vitro model. Additionally, neutralizing antibody against CXCL1 in a xenograft angiogenesis model resulted in inhibition of angiogenesis. Conclusions: CXCL1-induced regulation of angiogenesis has not been studied extensively in human cancers, thus these findings illustrate a novel contribution of CXCL1 interactions in pathological angiogenesis. Therefore, the ability to selectively modulate CXCL1, specifically in tumoral angiogenesis, may promote the development of novel oncologic therapeutic strategies.

Acute effects of 1,25-dihydroxycholecalciferol on human endothelial cell cultures

Bone ◽  
2009 ◽  
Vol 44 ◽  
pp. S354-S355
Author(s):  
C. Molinari⁎ ◽  
F. Uberti ◽  
E. Grossini ◽  
G. Vacca ◽  
M. Invernizzi ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Cultures ◽  
Human Endothelial Cell ◽  
Acute Effects ◽  
Endothelial Cell Cultures

The Effects of Shear Stress on Endothelial Cells at Hypothermic Temperatures

2002 ◽  
Author(s):  
John H. Slater ◽  
Shailendra Jain ◽  
Robin N. Coger ◽  
Charles Y. Lee
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Low Flow ◽  
Shear Stresses ◽  
Liver Sinusoids ◽  
Endothelial Cell Cultures ◽  
Shear Stress Response

Hypothermic machine perfusion preservation (MPP) has proven to be a successful technique for hypothermic kidney storage, however this technology has not successfully been applied to the liver. Recent research has indicated that the endothelial cells lining the liver sinusoids display rounding phenomena during MPP that is not fully understood. In order to gain a better understanding of endothelial cell shear stress response and the factors that induce rounding, a temperature-controlled micro-shear chamber has been designed and fabricated. The micro-shear chamber has been used to apply shear stresses, corresponding to those imposed during MPP, to rat liver primary endothelial cell cultures in order to form an understanding of how these stresses affect endothelial cell morphology. The chamber allows for the application of shear stresses ranging from 0.2 ± .01 dynes/cm2 to 2.3 ± 0.3 dynes/cm2, corresponding to what occurs during MPP.] Twenty-four hour in vitro experiments with shear stresses ranging from 0 to 1.49 dynes/cm2 at 4 °C were conducted in order to replicate in vivo conditions of the liver during hypothermic MPP. It has been demonstrated that endothelial cell rounding increases with increasing shear and can be prevented by utilizing low flow rates.

Adenosine stimulates proliferation of human endothelial cells in culture

1993 ◽  
Vol 265 (1) ◽  
pp. H131-H138 ◽  
Author(s):  
M. F. Ethier ◽  
V. Chander ◽  
J. G. Dobson
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Growth ◽  
Cell Cultures ◽  
Umbilical Vein ◽  
Fibroblast Cell ◽  
Human Endothelial Cells ◽  
Cell Counts ◽  
Endothelial Cell Cultures ◽  
Endothelial Cell Growth

The effect of adenosine on proliferation of human endothelial cells was investigated by adding adenosine to the medium of cultures derived from human umbilical veins. Cell counts on cultures grown in 10 microM adenosine for 4–7 days were 41–53% greater than counts from control cultures. In contrast, 10 microM adenosine had no effect on growth of a human fibroblast cell strain (IMR-90). Neither inosine nor 2',5'-dideoxyadenosine influenced endothelial cell growth at concentrations of 0.1 or 10 microM. Addition of adenosine deaminase abolished the proliferative effect of added adenosine and inhibited proliferation by 16% in control cultures, suggesting that endogenous adenosine may enhance proliferation in culture. The adenosine receptor antagonist, 8-phenyltheophylline, at 0.1 and 1.0 microM blocked the enhanced proliferation caused by 10 microM adenosine. Addition of 10 microM adenosine enhanced DNA synthesis in endothelial cell cultures as indicated by an increased incorporation of [3H]thymidine into acid-insoluble cell material. The results indicate that addition of physiological concentrations of adenosine to human umbilical vein endothelial cell cultures stimulates proliferation, possibly via a surface receptor, and suggest that adenosine may be a factor for human endothelial cell growth and possibly angiogenesis.

Abstract 73: Atrial Fibrillation-induced Changes in Left Atrial Hemodynamics Directly Impact the Thrombotic Potential of Human Primary Endothelial Cell Cultures

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Brian R Wamhoff ◽  
Michael B Simmers ◽  
Zhu Chen ◽  
Yiming Xu ◽  
Ling-jie Kong ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Sinus Rhythm ◽  
Cell Cultures ◽  
Left Atrial ◽  
Cell Phenotype ◽  
Shear Forces ◽  
Endothelial Cell Cultures ◽  
Aortic Endothelial

Thrombus formation in the left atrial appendage (LAA) of the heart is a source of stroke risk in patients with atrial fibrillation (Afib). Strategies to prevent thromboembolism from the LAA via restoration of normal rhythm or prevention of clot formation are limited by lack of adequate human surrogate systems that recapitulate the biology ex vivo. Endothelial cell phenotype and function in blood vessels and chambers of the heart are regulated in part by regional hemodynamics. Blood flow shear forces in the LAA are substantially altered during Afib. Thus, we hypothesized that Afib-induced alterations in hemodynamics directly impacts the thrombotic potential of the endothelium in the LAA. To test this, human primary aortic endothelial cell cultures were primed under hemodynamic shear forces simulating the human LAA during normal sinus rhythm for 24 hrs and continued under sinus rhythm or switched to simulate Afib for an additional 24 hrs. Compared to sustained sinus rhythm, Afib hemodynamics suppressed genes (qRTPCR) that define a healthy/quiescent endothelial cell phenotype (e.g. KLF2 and NOS3/eNOS) while inducing the pro-thrombotic gene F3 (tissue factor) and suppressing ADAMSTS13, MMP14 and TIMP2. To determine whether the observed molecular response produced a functional prothrombotic phenotype, hemodynamic primed aortic endothelial cells were exposed to dilute (~27% final concentration) human platelet-free plasma supplemented with Alexa488-labeled human fibrinogen, corn trypsin inhibitor and calcium. Cleavage of fibrinogen to fibrin and concomitant deposition on the endothelium was measured by quantitative confocal microscopy. When exposed to Afib hemodynamics, endothelial cells supported significant fibrin deposition that extended to greater depth (i.e., thicker) on the endothelium compared to sinus rhythm hemodynamics. In conclusion, we show for the first time a direct mechanistic link between changes in LAA hemodynamics associated with development of Afib and functional alterations in the thrombotic potential of the endothelium. This study produced a novel insight enabled by studying potential triggers of thrombosis in a context that more closely mimics the normal and pathological human in vivo environment.

Fibrin- and Collagen-Based Matrices Attenuate Inflammatory and Procoagulant Responses in Human Endothelial Cell Cultures Exposed toStaphylococcus aureus

2012 ◽  
Vol 18 (1-2) ◽  
pp. 147-156 ◽  
Author(s):  
Ruth Heying ◽  
Carolin Wolf ◽  
Henry Beekhuizen ◽  
Marie-Luise Moelleken ◽  
Stefan Jockenhoevel ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Cultures ◽  
Human Endothelial Cell ◽  
Endothelial Cell Cultures
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