Role of nitric oxide in the activation of NF-κB, AP-1 and NOS II expression in articular chondrocytes
| Autor: | Arsélio P. Carvalho, Alexandrina Ferreira Mendes, Maria do Carmo Lopes, Maria Margarida Caramona |
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| Rok vydání: | 2002 |
| Předmět: |
Cartilage
Articular Cytoplasm Blotting Western Immunology Nitric Oxide Synthase Type II Electrophoretic Mobility Shift Assay In Vitro Techniques S-Nitroso-N-Acetylpenicillamine Biology Nitric Oxide Nitric oxide chemistry.chemical_compound Chondrocytes Western blot medicine Animals Nitric Oxide Donors Electrophoretic mobility shift assay Northern blot Cells Cultured Cell Nucleus Pharmacology Dose-Response Relationship Drug medicine.diagnostic_test Activator (genetics) NF-kappa B Snap Blotting Northern Molecular biology Transcription Factor AP-1 Blot chemistry Cattle Nitric Oxide Synthase Signal transduction Interleukin-1 Signal Transduction |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 1023-3830 |
| Popis: | Objective and design: Determine the sources of nitric oxide (NO) and evaluate its role in the activation of nuclear Factor-kappaB (NF-κB) and activator protein-1 (AP-1) and in the expression of NO synthase II (NOS II), induced by interleukin-1β (IL-1).¶Material or subjects: Primary cultures of bovine articular chondrocytes.¶Treatment: The cells were treated with IL-1, 5 ng/ml with or without the NO donor S-nitroso-N-acetylpenicillamine (SNAP), in concentrations ranging from 10 to 300 μM.¶Methods: NF-κB and AP-1 activation were evaluated by electrophoretic mobility shift assay. Northern blot was used to detect NOS II mRNA levels and western blot to evaluate IκB-α, NOS I and NOS II protein levels.¶Results: Under basal conditions, chondrocytes expressed NOS I, which was lost upon IL-1 treatment. SNAP inhibited IL-1-induced NF-κB activation and NOS II expression. When added alone, SNAP induced AP-1 activation to approximately the same extent as IL-1.¶Conclusions: These results suggest that, in chondrocytes, NO is a key regulator of the signaling pathways leading from IL-1 to NF-κB and AP-1 activation and to the expression of genes that are involved in the pathophysiology of arthritic diseases. |
| Databáze: | OpenAIRE |
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