Modulation of Vascular Endothelium by Imatinib: A Study on the EA.hy 926 Endothelial Cell Line

In this study the EA.hy 926 endothelial cell line-simulating endothelial cells-was treated with imatinib in order to define a possible anti-angiogenic role for imatinib. Dose and time response experiments were performed. Cell morphology was studied, while migration efficiency, intercellular permeabi...

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Bibliographic Details
Published in:Journal of chemotherapy (Florence) 2006-02, Vol.18 (1), p.56-65
Main Authors: Vrekoussis, T., Stathopoulos, E.N., De Giorgi, U., Kafousi, M., Pavlaki, K., Kalogeraki, A., Chrysos, E., Fiorentini, G., Zoras, O.
Format: Article
Language:English
Subjects:
angiogenesis
Antibiotics. Antiinfectious agents. Antiparasitic agents
Antigens, CD
Antineoplastic Agents - pharmacology
apoptosis
Apoptosis - drug effects
Benzamides
Biological and medical sciences
Cadherins - metabolism
Cell Movement - drug effects
Cells, Cultured
endothelial cells
Endothelium, Vascular - cytology
Endothelium, Vascular - drug effects
Endothelium, Vascular - metabolism
Fluorescent Antibody Technique, Indirect
Humans
Imatinib
Imatinib Mesylate
Medical sciences
Neovascularization, Physiologic
Pharmacology. Drug treatments
Piperazines - pharmacology
Protein-Tyrosine Kinases - antagonists & inhibitors
Pyrimidines - pharmacology
Receptor, Platelet-Derived Growth Factor alpha - metabolism
Receptor, Platelet-Derived Growth Factor beta - metabolism
VE-cadherin
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Summary:In this study the EA.hy 926 endothelial cell line-simulating endothelial cells-was treated with imatinib in order to define a possible anti-angiogenic role for imatinib. Dose and time response experiments were performed. Cell morphology was studied, while migration efficiency, intercellular permeability and VE-cadherin expression were assayed, both in the presence and in the absence of imatinib. Imatinibinduced EA.hy 926 cell apoptosis was also examined. Results showed that imatinib reduced the endothelial cell population, changed cell monolayer morphology and reduced cell-to-cell cohesiveness. Migration efficiency was significantly decreased while intercellular permeability was 2.76-fold increased in the presence of imatinib. Indirect immunofluorescence microscopy showed nearly complete down-regulation of VE cadherin in imatinib-treated cells. Furthermore, apoptotic activity was detected in imatinib-treated cells. Altogether our results support an antiangiogenic profile for imatinib that possibly contributes to its therapeutic potential.
ISSN:1120-009X
1973-9478
DOI:10.1179/joc.2006.18.1.56