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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Cottin, T. Tsigkos, S. Waldmann, H. Giannis, A. Gourzoulidou, E. Pyriochou, A. Papapetropoulos, A. Vassilakopoulos, T. Zhou, Z. Roussos, C. |
| Description | Author Affiliation: Pyriochou A ( Laboratory of Molecular Pharmacology, Department of Pharmacy, University of Patras, Patras, Greece.) |
| Abstract | BACKGROUND AND PURPOSE: Angiopoietins (Ang) are crucial for new blood vessel formation and exert their effects by acting on the Tie2 receptor. We have recently described a sulindac analogue 2-((1E,Z)-1-benzylidene-5-bromo-2-methyl-1H-inden-3-yl)acetic acid; termed C-18 from now onwards) that inhibits Tie2 receptor activity in kinase assays in vitro. Here, we have assessed the ability of C-18 to inhibit angiogenesis-related properties of endothelial cells and tested its selectivity for the Tie2 receptor. EXPERIMENTAL APPROACH: For in vitro experiments human umbilical vein endothelial cells (HUVEC) were used. Proliferation was measured using the MTT assay; migration assays were performed in a modified Boyden chamber and tube-like structure formation was determined on matrigel. The effects of C-18 in vivo were evaluated in the chicken chorioallantoic membrane (CAM). KEY RESULTS: Pre-treatment of HUVEC with C-18 blocked Ang-1-stimulated migration, but also abolished vascular endothelial cell growth factor (VEGF)- and fibroblast growth factor 2-induced responses. Incubation with C-18 inhibited serum-induced proliferation in a concentration-dependent manner; C-18 was, however, without effect on Ang-1-induced survival. In addition, we observed that C-18 did not inhibit ligand-induced receptor phosphorylation of Tie2 or VEGFR2. On the other hand, C-18 blocked activation of members of the mitogen-activated protein kinase family and of the Ser/Thr kinase Akt induced by both VEGF and Ang-1. Furthermore, incubation of CAMs with C-18 led to a dose-dependent inhibition of vascular length. CONCLUSIONS AND IMPLICATIONS: C-18 did not act as a Tie2 inhibitor, as originally thought, but rather inhibited growth factor-stimulated signalling pathways that regulate endothelial cell migration and potently reduces neovascularization in vivo. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 8 |
| Volume Number | 152 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 2007-12-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Angiogenesis Inhibitors Pharmacology Endothelial Cells Drug Effects Receptor, TIE-2 Angiopoietin-1 Antagonists & Inhibitors Animals Cell Movement Cell Proliferation Cell Survival Cells, Cultured Chick Embryo Chorioallantoic Membrane Metabolism Dose-Response Relationship, Drug Fibroblast Growth Factor 2 Mitogen-Activated Protein Kinases Phosphorylation Protein-Serine-Threonine Kinases Signal Transduction Sulindac Administration & Dosage Umbilical Veins Vascular Endothelial Growth Factor A Research Support, Non-U.S. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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