FACTORS INFLUENCING THE EFFECT OF THE SOLUBLE IL-6 RECEPTOR ON IL-6 RESPONSES IN HepG2 HEPATOCYTES
| Autor: | Roland Blanqué, Claudine Soria, Colin R Gardner, J. Paysant, Marc Vasse, Jeannette Soria |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
medicine.medical_specialty
Carcinoma Hepatocellular media_common.quotation_subject Immunology Endogeny Biology Biochemistry Dexamethasone Internal medicine Tumor Cells Cultured medicine Humans Immunology and Allergy Internalization Beta (finance) Interleukin 6 Receptor Molecular Biology media_common Interleukin-6 Cell Membrane Liver Neoplasms Hematology Glycoprotein 130 Ligand (biochemistry) Receptors Interleukin-6 Endocrinology Gene Expression Regulation Interleukin-6 receptor biology.protein Signal Transduction |
| Zdroj: | Cytokine. 12:774-779 |
| ISSN: | 1043-4666 |
| DOI: | 10.1006/cyto.1999.0649 |
| Popis: | The soluble IL-6 receptor (sIL-6R) can increase IL-6-induced signalling by forming a complex with IL-6 and membrane-bound gp130 (the receptor beta chain which transduces signals). The conditions affecting this response to sIL-6R were studied using fibrinogen release from HepG2 hepatocytes. Exogenous sIL-6R had no effect alone or in the presence of a submaximal concentration of IL-6, but increased responses to supramaximal IL-6 concentrations in a concentration-related manner. Dexamethasone increased the expression of the membrane IL-6R and endogenous sIL6R release, and increased responses to supramaximal but not submaximal IL-6 concentrations. The amount of endogenous sIL-6R released is relatively small and is unlikely to influence the effects of the exogenous sIL-6R. The observed concentration-related decrease in sIL-6R production in the presence of IL-6 may indicate internalization of ligand/receptor complexes. This would significantly decrease the amount of IL-6R (soluble or membrane) available for signalling and limit continued functional response later in the cultures. These data indicate that the major factor influencing responses to exogenous sIL-6R is an excess of IL-6 which is necessary to form complexes with the sIL-6R, which can then interact with gp130 to increase signalling. |
| Databáze: | OpenAIRE |
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