Abstract |
In an attempt to elucidate the mechanism(s) of action of thalidomide, a reportedly antiangiogenic molecule recently tested in the treatment of relapsing malignant gliomas, we performed an in vitro study on the following parameters: (a) effect of thalidomide on proliferation of endothelial cells; (b) effect of thalidomide on expression of alpha(v) beta3 integrin on the surface of endothelial cells; (c) effect of thalidomide on the release by endothelial cells of MMP-2, IL-8 and TNF-alpha. The results show that thalidomide inhibits endotelial cell proliferation induced by bFGF and VEGF, more so if the cells are grown on vitronectin; moreover, treatment with thalidomide reduces the release of MMP-2 and IL-8 by endothelial cells, suggesting a further pathway for the antiangiogenic activity of drug. On the other hand, thalidomide does not modify expression of alpha(v)beta3 on endothelial cells.
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Authors | M Gelati, E Corsini, S Frigerio, B Pollo, G Broggi, D Croci, A Silvani, A Boiardi, A Salmaggi |
Journal | Journal of neuro-oncology
(J Neurooncol)
Vol. 64
Issue 3
Pg. 193-201
(Sep 2003)
ISSN: 0167-594X [Print] United States |
PMID | 14558594
(Publication Type: Journal Article)
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Chemical References |
- Angiogenesis Inhibitors
- Endothelial Growth Factors
- Integrin alphaVbeta3
- Intercellular Signaling Peptides and Proteins
- Interleukin-8
- Lymphokines
- Receptors, Cell Surface
- Tumor Necrosis Factor-alpha
- Vascular Endothelial Growth Factor A
- Vascular Endothelial Growth Factors
- Vitronectin
- Fibroblast Growth Factor 2
- Thalidomide
- Matrix Metalloproteinase 2
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Topics |
- Angiogenesis Inhibitors
(pharmacology)
- Cell Division
(drug effects)
- Cells, Cultured
- Endothelial Growth Factors
(physiology)
- Endothelium, Vascular
(cytology, drug effects, growth & development, metabolism)
- Fibroblast Growth Factor 2
(physiology)
- Humans
- Integrin alphaVbeta3
(metabolism)
- Intercellular Signaling Peptides and Proteins
(physiology)
- Interleukin-8
(metabolism)
- Lymphokines
(physiology)
- Matrix Metalloproteinase 2
(metabolism)
- Neovascularization, Pathologic
(prevention & control)
- Neovascularization, Physiologic
(drug effects)
- Receptors, Cell Surface
(metabolism)
- Thalidomide
(pharmacology)
- Tumor Necrosis Factor-alpha
(metabolism)
- Umbilical Veins
(cytology)
- Vascular Endothelial Growth Factor A
- Vascular Endothelial Growth Factors
- Vitronectin
(physiology)
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