ICAM-1 and VCAM-1 expression induced by TNF-alpha are inhibited by a glutathione peroxidase mimic
| Autor: | Jean Chaudiere, Marc Moutet, Evelyne Coudrier, Sophie Darquenne, Patrizia d’Alessio |
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| Rok vydání: | 1998 |
| Předmět: |
Azoles
Umbilical Veins Cytochalasin D Vascular Cell Adhesion Molecule-1 Isoindoles Biochemistry chemistry.chemical_compound Physiology (medical) Organoselenium Compounds Humans VCAM-1 Cycloheximide Cell adhesion Cytoskeleton Selenium Compounds Cells Cultured Cell Size chemistry.chemical_classification ICAM-1 Glutathione Peroxidase Cell adhesion molecule Tumor Necrosis Factor-alpha Glutathione peroxidase Molecular Mimicry Intercellular Adhesion Molecule-1 Actins Cell biology chemistry Tumor necrosis factor alpha Endothelium Vascular Drug Antagonism |
| Zdroj: | Free radical biologymedicine. 24(6) |
| ISSN: | 0891-5849 |
| Popis: | Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are respectively involved in the endothelial recruitment of neutrophils, and in that of lymphocytes or tumor cells, in response to specific signals. We have used the glutathione peroxidase (GPx) mimic BXT-51072 to assess the possibility that endogenous hydroperoxides play a role in the tumor necrosis factor-alpha (TNFalpha)-induced expression of ICAM-1 and VCAM-1 by monolayers of human endothelial cells. The GPx mimic BXT-51072 strongly inhibits the TNFalpha-induced and cycloheximide-sensitive expression of ICAM-1 and VCAM-1. It also inhibits the TNFalpha-induced reorganization of the actin network and the associated formation of stress fibers. Actin reorganization induced by cytochalasin D treatment did not inhibit ICAM-1 expression. Our results are compatible with specific and synergistic effects of endogenous hydroperoxides on the biosynthesis and processing of cell adhesion molecules and cytoskeleton components. |
| Databáze: | OpenAIRE |
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