Regulation of granulocyte colony-stimulating factor gene expression by interleukin-17
| Autor: | Satwant K. Narula, Jay S. Fine, Xiao-Yan Cai, Carl P. Gommoll, Luminita Justice |
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| Rok vydání: | 1998 |
| Předmět: |
Lipopolysaccharides
Stromal cell Immunology Biology 3T3 cells Cell Line Proinflammatory cytokine Mice Granulocyte Colony-Stimulating Factor Gene expression medicine Animals Immunology and Allergy Cycloheximide Enzyme Inhibitors Protein Synthesis Inhibitors Regulation of gene expression Interleukins Macrophages Monocyte Interleukin-17 3T3 Cells Genistein Molecular biology Haematopoiesis medicine.anatomical_structure Gene Expression Regulation Cytokines Mitogens Granulocyte colony-stimulating factor receptor |
| Zdroj: | Immunology Letters. 62:51-58 |
| ISSN: | 0165-2478 |
| DOI: | 10.1016/s0165-2478(98)00027-3 |
| Popis: | Interleukin-17 (IL-17) has been previously reported to induce stromal cells to produce a number of hematopoietic and proinflammatory cytokines, including granulocyte colony-stimulating factor (G-CSF). Here, we have evaluated the mechanisms responsible for the augmentation of G-CSF gene expression by IL-17, using the murine 3T3 fibroblast cell line. Treatment of 3T3 cells, but not primary bone marrow-derived macrophages or murine monocyte/macrophage cell lines, resulted in increased steady-state G-CSF mRNA levels within 2-4 h and augmented G-CSF protein production. The combination of IL-17 and LPS enhanced G-CSF expression in an additive fashion. Stability studies revealed that IL-17 stabilized G-CSF mRNA levels, with a t1/2 of 4 h, compared to a t1/2 of less than 2 h in medium or LPS-treated cells. Induction of G-CSF expression in 3T3 cells by IL-17 did not appear to require tyrosine kinase activation or de novo protein synthesis. These studies indicate that post-transcriptional mechanisms play an important role in IL-17-induced G-CSF expression in fibroblasts and suggest that IL-17 may be useful for further delineating mechanisms of G-CSF gene regulation. |
| Databáze: | OpenAIRE |
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