The Angiogenesis Inhibitor AGM-1470 Selectively Increases E-Selectin

The levels of E-selectin mRNA and protein were analyzed in bovine capillary cells treated with or without the angiogenesis inhibitor AGM-1470 (also known as TNP-470). Cells treated with AGM-1470 had a two- to sevenfold (median fivefold) increase in E-selectin mRNA compared with little or no increase...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 1996-08, Vol.225 (1), p.141-145
Main Authors: Budson, Andrew E., Ko, Lydia, Brasel, Chris, Bischoff, Joyce
Format: Article
Language:English
Subjects:
Adrenal Cortex - blood supply
Animals
Antibiotics, Antineoplastic - pharmacology
Antigens, Differentiation, Myelomonocytic - biosynthesis
Capillaries
Cattle
Cell Adhesion Molecules - biosynthesis
Cyclohexanes
E-Selectin - biosynthesis
Endothelium, Vascular - cytology
Endothelium, Vascular - drug effects
Endothelium, Vascular - physiology
Gene Expression - drug effects
Neovascularization, Physiologic - drug effects
P-Selectin - biosynthesis
Platelet Endothelial Cell Adhesion Molecule-1
Protein Biosynthesis
RNA, Messenger - biosynthesis
Sesquiterpenes - pharmacology
Transcription, Genetic
Vascular Cell Adhesion Molecule-1 - biosynthesis
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Summary:The levels of E-selectin mRNA and protein were analyzed in bovine capillary cells treated with or without the angiogenesis inhibitor AGM-1470 (also known as TNP-470). Cells treated with AGM-1470 had a two- to sevenfold (median fivefold) increase in E-selectin mRNA compared with little or no increase in P-selectin, PECAM-1 and VCAM-1 mRNA. E-selectin protein was also significantly increased after exposure to AGM-1470. In contrast, there was no detectable effect on PECAM-1 protein. The increase in E-selectin mRNA and protein was always greater with subconfluent growing cells than with confluent cells. This apparent resistance of confluent endothelial cells to AGM-1470 may be relevant to its specificityin vivo.The fact that the effect of AGM-1470 on E-selectin is relatively selective for subconfluent growing cells may provide a clue as to how AGM-1470 is able to both reversibly inhibit endothelial cell proliferationin vitroand inhibit tumor growthin vivowithout apparent effects to quiescent endothelium.
ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.1996.1143