Tumor Necrosis Factor (TNF)-α and Interleukin (IL)-1β Down-regulate Intercellular Adhesion Molecule (ICAM)-2 Expression on the Endothelium
| Autor: | Fiona McLaughlin, Carmel M.T. Horgan, Julian E. Beesley, Brian Hayes, Callum J. Campbell, Anna M. Randi |
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| Rok vydání: | 1998 |
| Předmět: |
Time Factors
Endothelium medicine.medical_treatment Molecular Sequence Data Down-Regulation Umbilical Cord Proinflammatory cytokine Antigens CD Genes Reporter Sequence Homology Nucleic Acid E-selectin medicine Humans Luciferases Lymphotoxin-alpha Cells Cultured Inflammation Microscopy Confocal Base Sequence Dose-Response Relationship Drug biology Reverse Transcriptase Polymerase Chain Reaction Tumor Necrosis Factor-alpha Cell adhesion molecule Chemistry Soluble cell adhesion molecules Antibodies Monoclonal General Medicine Blotting Northern Flow Cytometry Intercellular adhesion molecule Molecular biology Cell biology medicine.anatomical_structure Cytokine Microscopy Fluorescence biology.protein Tumor necrosis factor alpha Endothelium Vascular Cell Adhesion Molecules Interleukin-1 |
| Zdroj: | Cell Adhesion and Communication. 6:381-400 |
| ISSN: | 1029-2314 |
| DOI: | 10.3109/15419069809109147 |
| Popis: | Leukocyte recruitment is a crucial step in inflammation. Inflammatory stimuli upregulate the expression of some endothelial adhesion molecules, such as E-selectin or ICAM-1, but not of others such as ICAM-2. ICAM-2, a constitutively expressed endothelial ligand for beta2 integrins LFA-1 and Mac-1, is involved in leukocyte adhesion to resting endothelium and in transmigration in vitro, however its role in inflammation is unclear. We have studied the effect of TNF-alpha and IL-1beta on ICAM-2 expression on human umbilical vein endothelial cells (HUVECs). Prolonged treatment (24 h) of HUVECs with TNF-alpha (10 ng/ml) or IL-1beta (34 ng/ml) reduced ICAM-2 surface expression to 50% of control, while interferon (IFN)-gamma had no effect. The loss in ICAM-2 surface expression correlated with a reduction of ICAM-2 mRNA to approximately 40% of control after 24 h of cytokine treatment. The activity of an ICAM-2 promoter reporter plasmid transfected into HUVECs was down-regulated by TNF-alpha and IL-1beta to similar values. Thus inflammatory cytokines inhibit ICAM-2 transcription, despite the absence of known cytokine-responsive elements in the promoter. Immunocytochemistry on HUVEC monolayers showed that ICAM-2 expression, mainly at the cell junctions in resting cells, was markedly decreased by cytokine treatment. This data suggest that ICAM-2 expression on the endothelium may be regulated during inflammation. |
| Databáze: | OpenAIRE |
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