Human Endothelial Cells Modulate Thrombus Formation in an In Vitro Model of Platelet-Vessel Wall Interactions

1990 ◽  
pp. 45-52
Author(s):  
T. H. Müller ◽  
W. G. Eisert
Keyword(s):  
Endothelial Cells ◽  
Vessel Wall ◽  
In Vitro Model ◽  
Thrombus Formation ◽  
Human Endothelial Cells ◽  
Vitro Model ◽  
Wall Interactions

Autocrine Control of Angiogenesis by Endogenous Acetylcholine in an In Vitro Model Using Human Endothelial Cells

2015 ◽  
Vol 65 (5) ◽  
pp. 508-515 ◽  
Author(s):  
Stefan Dhein ◽  
Alice Wermke ◽  
Sandy von Salisch ◽  
Franziska Schlegel ◽  
Holger Stepan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
In Vitro Model ◽  
Human Endothelial Cells ◽  
Autocrine Control ◽  
Vitro Model

Stimulation of prostaglandin synthesis by human endothelial cells exposed to hypoxia

1993 ◽  
Vol 264 (4) ◽  
pp. C866-C874 ◽  
Author(s):  
C. Michiels ◽  
T. Arnould ◽  
I. Knott ◽  
M. Dieu ◽  
J. Remacle
Keyword(s):  
Endothelial Cells ◽  
Calcium Concentration ◽  
In Vitro Model ◽  
Cytosolic Calcium ◽  
Cyclooxygenase Inhibitors ◽  
Resting Cells ◽  
Human Endothelial Cells ◽  
Vitro Model

In ischemic organs, arachidonic acid (AA) metabolites and mostly prostaglandins (PGs) have been found to be released in high amounts. The mechanism for this AA metabolism activation and its physiological implications are not clear. Because endothelial cells are an important source of PGs and because they seem to be very rapidly affected by ischemia, we developed an in vitro model where human endothelial cells were submitted to hypoxia. An important specific activation of phospholipase A2 was observed during hypoxia, which was concomitant with a rise in cytosolic calcium concentration. Endothelial cells synthetize in normal conditions as a mean 1.42, 1.00, 7.69, and 26.92 ng/mg proteins of, respectively, PGE2, PGD2, PGF2 alpha, PGI2. An important increase of about five- to ninefold in the synthesis of the four PGs was observed during hypoxia, which followed the same kinetics as the PLA2 activation. This increase in PG synthesis was sensitive to cyclooxygenase inhibitors. During reoxygenation, PG synthesis decreased back to the basal level of resting cells, suggesting that cells were able to recover their homeostasis after hypoxia. These observations indicate that endothelial cells exposed to oxygen deprivation are a major source of PGs and could contribute to the high amounts of PG released in vivo in ischemic organs.

scholarly journals Generation of a Novel In Vitro Model to Study Endothelial Dysfunction from Atherothrombotic Specimens

2021 ◽  
Author(s):  
Susan Gallogly ◽  
Takeshi Fujisawa ◽  
John D. Hung ◽  
Mairi Brittan ◽  
Elizabeth M. Skinner ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
In Vitro Model ◽  
Umbilical Vein ◽  
Coronary Syndrome ◽  
Coronary Endothelial Cells ◽  
Vitro Model ◽  
Umbilical Vein Endothelial Cells

Abstract Purpose Endothelial dysfunction is central to the pathogenesis of acute coronary syndrome. The study of diseased endothelium is very challenging due to inherent difficulties in isolating endothelial cells from the coronary vascular bed. We sought to isolate and characterise coronary endothelial cells from patients undergoing thrombectomy for myocardial infarction to develop a patient-specific in vitro model of endothelial dysfunction. Methods In a prospective cohort study, 49 patients underwent percutaneous coronary intervention with thrombus aspiration. Specimens were cultured, and coronary endothelial outgrowth (CEO) cells were isolated. CEO cells, endothelial cells isolated from peripheral blood, explanted coronary arteries, and umbilical veins were phenotyped and assessed functionally in vitro and in vivo. Results CEO cells were obtained from 27/37 (73%) atherothrombotic specimens and gave rise to cells with cobblestone morphology expressing CD146 (94 ± 6%), CD31 (87 ± 14%), and von Willebrand factor (100 ± 1%). Proliferation of CEO cells was impaired compared to both coronary artery and umbilical vein endothelial cells (population doubling time, 2.5 ± 1.0 versus 1.6 ± 0.3 and 1.2 ± 0.3 days, respectively). Cell migration was also reduced compared to umbilical vein endothelial cells (29 ± 20% versus 85±19%). Importantly, unlike control endothelial cells, dysfunctional CEO cells did not incorporate into new vessels or promote angiogenesis in vivo. Conclusions CEO cells can be reliably isolated and cultured from thrombectomy specimens in patients with acute coronary syndrome. Compared to controls, patient-derived coronary endothelial cells had impaired capacity to proliferate, migrate, and contribute to angiogenesis. CEO cells could be used to identify novel therapeutic targets to enhance endothelial function and prevent acute coronary syndromes.

Platelets and Endothelial Cells Act in Concert to Delay Thrombolysis – Evidence from an In Vitro Model of the Human Occlusive Thrombus

1998 ◽  
Vol 79 (03) ◽  
pp. 602-608 ◽  
Author(s):  
W. G. Jerome ◽  
S. Handt ◽  
R. R. Hantgan
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
In Vitro Model ◽  
Umbilical Vein ◽  
Plasminogen Activator Inhibitor ◽  
Genetically Engineered ◽  
Cellular Mechanisms ◽  
Vitro Model ◽  
Activator Inhibitor

SummaryThe molecular and cellular mechanisms that over a period of hours render a human thrombus progressively resistant to fibrinolysis have been probed with a novel in vitro model. The kinetics of clot formation and fibrinolysis were monitored by laser light scattering with platelet-rich model thrombi contained in cylindrical flow chambers. In selected experiments, human umbilical vein endothelial cells were also cultured to confluence on the inner walls of these “glass blood vessels”. Following an “aging” period (0.5, 2 or 4 h), each thrombus was gently perfused with a bolus of plasminogen/recombinant tissue plasminogen activator to induce fibrinolysis. Platelets delayed lysis of 2 h-aged thrombi by ~70% and (non-stimulated) endothelial cells by ~30%, compared to cell-free control clots. However, even greater lytic delays (~260%) resulted when both vascular cells were present in the same 2 h-aged thrombus. In contrast, rapid lysis was consistently achieved with R298E,R299E t-PA, a genetically engineered plasminogen activator that is insensitive to inhibition by plasminogen activator inhibitor type 1. These observations suggest platelets and endothelial cells act in concert to enrich the fibrin scaffold of an aging human thrombus in plasminogen activator inhibitor. We propose that the presence of both platelets and endothelial cells may contribute to progressive thrombolytic resistance.

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