Alginate-gelatin encapsulation of human endothelial cells promoted angiogenesis in in vivo and in vitro milieu

2017 ◽  
Vol 114 (12) ◽  
pp. 2920-2930 ◽  
Author(s):  
Sorour Nemati ◽  
Aysa Rezabakhsh ◽  
Ali Baradar Khoshfetrat ◽  
Alireza Nourazarian ◽  
Çığır Biray Avci ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Human Endothelial Cells

scholarly journals Annexin 5 as a potential regulator of annexin 1 phosphorylation by protein kinase C. In vitro inhibition compared with quantitative data on annexin distribution in human endothelial cells

1993 ◽  
Vol 292 (3) ◽  
pp. 759-765 ◽  
Author(s):  
P Raynal ◽  
F Hullin ◽  
J M F Ragab-Thomas ◽  
J Fauvel ◽  
H Chap
Keyword(s):  
Endothelial Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Inhibitory Effect ◽  
Human Endothelial Cells ◽  
Annexin 1 ◽  
Kinase C ◽  
Vitro Effect

In vitro phosphorylation of annexin 1 by purified rat brain protein kinase C (PKC) has been studied in the presence of annexin 5, which is not a substrate for PKC. Annexin 5 promoted a dose-dependent inhibition of annexin 1 phosphorylation, which could be overcome by increasing the concentration of phosphatidylserine (PtdSer). In addition, a close relationship was found between the amount of PtdSer uncovered by annexin 5 and the residual phosphorylation of annexin 1. These data fit with the ‘surface depletion model’ explaining the antiphospholipase activity of annexins. In order to check the possibility that the in vitro effect of annexin 5 could be of some physiological relevance, annexins 1, 2, and 5, as well as the light chain of calpactin 1 (p11), have been quantified in human endothelial cells by measuring the radioactivity bound to the proteins after Western blotting with specific antibodies and 125I-labelled secondary antibody. Our data indicate that annexins 1 and 5, PKC and PtdSer are present in human endothelial cells in relative amounts very similar to those used in vitro under conditions permitting the detection of the inhibitory effect of annexin 5. Since annexin 1 remained refractory to PKC-dependent phosphorylation in intact cells, we suggest that annexin 5 might exert its inhibitory effect towards PKC in vivo, provided that its binding to phospholipids can occur at physiological (micromolar) concentrations of Ca2+. This was previously shown to occur in vitro using phosphatidylethanolamine/phosphatidic acid vesicles [Blackwood and Ernst (1990) Biochem. J. 266, 195-200]. Using identical assay conditions, which also allowed expression of PKC activity, annexin 5 again inhibited annexin 1 phosphorylation without interfering with PKC autophosphorylation. These data suggest that annexins 1 and 5 might interact with each other on the lipid surface, resulting in a specific inhibition of annexin 1 phosphorylation by PKC. Whether a similar mechanism also occurs in vivo remains to be determined.

scholarly journals Inflammation Determines the Pro-Adhesive Properties of High Extracellular D-Glucose in Human Endothelial Cells In Vitro and Rat Microvessels In Vivo

PLoS ONE ◽  
2010 ◽  
Vol 5 (4) ◽  
pp. e10091 ◽  
Author(s):  
Verónica Azcutia ◽  
May Abu-Taha ◽  
Tania Romacho ◽  
Marta Vázquez-Bella ◽  
Nuria Matesanz ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Human Endothelial Cells ◽  
Adhesive Properties

scholarly journals Growth inhibition of human endothelial cells by the phyto-oestrogen biochanin A, a metabolite of genistein

2001 ◽  
Vol 85 (5) ◽  
pp. 615-620 ◽  
Author(s):  
Chingwen Ying ◽  
Jih-Tay Hsu ◽  
Show-Chi Shieh
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Cell Density ◽  
Biochanin A ◽  
Human Endothelial Cells ◽  
Growth Inhibitory ◽  
Dose Dependent Fashion ◽  
Regulatory Effects

This study examined the growth regulatory effects of a phyto-oestrogen, biochanin A, on a transformed human endothelial cell line ECV304 in vitro. Biochanin A was found to inhibit cell proliferation in a dose-dependent fashion and this effect was influenced by the concentration of serum present in the culture medium. In the absence of serum, the calculated IC50 of biochanin A was 0.18 ± 0.1 μM COMPARED TO AN IC50 OF 35±5 Μm at 10 % serum. At low cell density, the growth inhibitory effects of biochanin A were more evident than at high cell density. Co-administration of a synthetic oestrogen diethylstilboestrol with biochanin A did not suppress the growth regulatory effects of biochanin A treatment. We conclude that biochanin A inhibits the cell proliferation of human endothelial cells at concentrations that are physiologically achievable in vivo and that this effect may play an important role in the cancer-preventing activity of the phyto-oestrogens.

Either exogenous or endogenous fibronectin can promote adherence of human endothelial cells

1986 ◽  
Vol 82 (1) ◽  
pp. 263-280
Author(s):  
R.A. Clark ◽  
J.M. Folkvord ◽  
L.D. Nielsen
Keyword(s):  
Endothelial Cells ◽  
Wound Repair ◽  
Cell Types ◽  
Culture Conditions ◽  
Collagen Type Iv ◽  
Human Endothelial Cells ◽  
Small Vessels ◽  
Microvascular Cells

Recently, we have presented evidence that proliferating blood vessels produce and deposit fibronectin in situ during the angiogenesis of wound repair. This report extends these observations by demonstrating that human endothelial cells from both large and small vessels depend on fibronectin for their adherence in vitro. Endothelial cells were grown from human umbilical veins (HUVEC) by the method of Gimbrone and from the microvasculature of human omentum by the method of Kern, Knedler and Eckel. Second-passage cells were plated into microtitre wells that had been coated with 100 micrograms ml-1 of fibronectin, types I and III collagen, type IV collagen or laminin. After a 3-h incubation, adherent cells were solubilized with Zap-Isoton and quantified on a Coulter Counter. Under normal culture conditions HUVEC showed no preference for fibronectin substrates while microvascular cells always demonstrated a striking preference for fibronectin substrates. However, when HUVEC were exposed to 2.5 or 25 micrograms ml-1 of cycloheximide for 4 h before and during the adherence assays, the adherence to fibronectin was 50–200% greater than to types I and III collagen. Immunofluorescence studies showed that while HUVEC expressed a large quantity of surface fibronectin, microvascular cells expressed very little. Metabolic labelling studies confirmed that HUVEC cultures had substantial quantities of fibronectin in their cell layer while microvascular cells did not. In antibody blocking experiments, preincubation of fibronectin-coated surfaces with anti-fibronectin antibodies totally blocked microvascular cell adhesion but only abrogated HUVEC adherence by 50%, presumably since these latter cells were able to deposit additional fibronectin onto the surface during the 3 h assay period. In the presence of cycloheximide anti-fibronectin antibodies totally blocked HUVEC adherence. These results demonstrate that both endothelial cell types rely, at least in part, on fibronectin for adherence in vitro. HUVEC can synthesize, secrete and deposit enough fibronectin for their adherence in vitro, while microvascular cells rely on an exogenous source of fibronectin under these culture conditions. Thus, the increased blood vessel fibronectin observed during angiogenesis in vivo may mediate adherence of the proliferating and migrating endothelial cells.

INFLUENCE OF BACTERIAL ENDOTOXIN ON RADIATION-INDUCED ACTIVATION OF HUMAN ENDOTHELIAL CELLS IN VITRO AND IN VIVO

1997 ◽  
Vol 64 (9) ◽  
pp. 1370-1373 ◽  
Author(s):  
Heidrun Lindner ◽  
Ernst Holler ◽  
Armin Gerbitz ◽  
Judith P. Johnson ◽  
Georg W. Bornkamm ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Bacterial Endotoxin ◽  
Human Endothelial Cells ◽  
Radiation Induced

Thrombin induces Contraction And increased 51-Cr Release from Cultured Human Endothelial Cells

1979 ◽  
Author(s):  
K.S. Galdal ◽  
S.A. Evensen
Keyword(s):  
Endothelial Cells ◽  
Calf Serum ◽  
Linear Increase ◽  
Foetal Calf Serum ◽  
Human Endothelial Cells ◽  
Trypan Blue Exclusion ◽  
Trypan Blue Exclusion Test ◽  
Release Assay

Injury to human endothelial cells(EC) in primary culture was evaluated by a 51-Cr release assay, phase contrast microscopy and the trypan blue exclusion test. Normal integrity of EC, was maintained and 51-Cr release showed a slow linear increase during 24h incubation with either RPMI 1640 supplemented with 20% foetal calf serum, glutamine and antibiotics(SCM) or normal human serum(NHS). Thrombin in a concentration as low as 0.1 IU/ml induced obvious contraction of EC incubated in SCM, but the cells remained fixed to the bottom of the wells. Cell contraction was maximal after 15min and disappeared within 4h. 51-Cr release increased 2-3 fold within a few minutes and remained increased during an incubation period of 4h. The injurious effect of thrombin was inhibited in SCM containing hirudin(l.7 u/ml) or in NHS. ADP(10-5 M), endotoxin (0.1mg/ml) and 5 vasoactive agents adrenalin 5.5 10-5, noradrenalin 5.9 10-5 M, histamine 9.10-4 M, bradykinin 7.5 10-7 M and serotonin 10-5 M) did not cause cellular injury. Cultured human EC are injured by thrombin. The other tested agents do not appear to induce direct injury in vitro, but may interact with cellular elements in the blood to produce the endothelial injury previously observed in vivo.

An In Vitro Toxicity Assay for Human Endothelial Cells

1988 ◽  
Vol 16 (1) ◽  
pp. 38-41
Author(s):  
Rosella Sbarbati ◽  
Maria Luisa Schinetti ◽  
Maria Scarlattini
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Umbilical Vein ◽  
Vascular Diseases ◽  
In Vitro Toxicity ◽  
Human Endothelial Cells ◽  
Experimental Conditions ◽  
Umbilical Vein Endothelial Cells

Cultured human endothelial cells can replace living animals in studying the toxic role of noxious agents in the pathogenesis of vascular diseases and in the elucidation of the mechanism of action of protective drugs. Preliminary data are presented which examine the effects that oxidative stress produces on human endothelial cells in vitro. Human umbilical vein endothelial cells were subjected to an anoxia-re-oxygenation treatment and tested for the production of Super Oxide Dismutase (SOD)-inhibitable superoxide radicals. The results show that under our experimental conditions endothelial cells produce oxygen-free radicals and that the generation reaches a maximum after an anoxic challenge of 20 minutes. We conclude that the in vitro system presented in this paper could be a suitable tool for further studies on the effects of oxidative stress on the vascular endothelium, which mimics the in vivo conditions of re-perfusion after heart ischemia.

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.

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