Tumor necrosis factor alpha enhances the expression of the interleukin (IL)-4 receptor alpha-chain on endothelial cells increasing IL-4 or IL-13-induced Stat6 activation
Autor: | Markus H. Heim, René Moser, Serena Lugli, Bruno Schnyder, Hansueli Etter, Rudolf A. Lutz, Hans-Pietro Eugster, Ningping Feng, Gerard Zurawski, Michèle Adam, Mat Yamage |
---|---|
Rok vydání: | 1997 |
Předmět: |
Models
Molecular Receptor complex Interleukin 5 receptor alpha subunit Interleukin 1 receptor type II Biology Vascular endothelial growth inhibitor Biochemistry Polymerase Chain Reaction Interleukin 10 receptor alpha subunit Cricetulus Antigens CD Cricetinae Animals Humans Molecular Biology Interleukin 12 receptor beta 1 subunit Interleukin-13 Tumor Necrosis Factor-alpha Cell Biology Receptors Interleukin Protein-Tyrosine Kinases Molecular biology Receptors Interleukin-4 Up-Regulation Enzyme Activation Interleukin 10 Spectrometry Fluorescence Trans-Activators Electrophoresis Polyacrylamide Gel Female Endothelium Vascular Interleukin-4 Interleukin 1 receptor type I STAT6 Transcription Factor Signal Transduction |
Zdroj: | The Journal of biological chemistry. 272(9) |
ISSN: | 0021-9258 |
Popis: | Functional receptors for interleukin (IL)-4 and IL-13 on endothelial cells consist of the 130-kDa IL-4 receptor alpha-chain (IL-4Ralpha) and a 65-75-kDa IL-13 binding subunit that are expressed in a ratio of about 1:3, respectively. The restricted number of IL-4Ralpha limits subunit heterodimerization and in turn receptor-mediated signaling. We report here, the effects of tumor necrosis factor alpha (TNF-alpha) on the expression of the receptor subunits for IL-4 and IL-13. By flow cytofluorometry and receptor-binding analysis of iodinated IL-4 and IL-13, stimulation with TNF-alpha-induced a 2-3-fold increase of the IL-4Ralpha expression. The up-regulation was also confirmed at the transcriptional level by reverse transcription-polymerase chain reaction. Radioligand cross-linking experiments revealed no change in the subunit composition of the TNF-alpha-induced receptor complex. Nevertheless, TNF-alpha stimulation led to increased activation of the IL-4-specific signal transducers and activators of transcription protein (Stat6) by IL-4 and IL-13. Thus, TNF-alpha corrects the subunit imbalance of the endothelial IL-4.IL-13 receptor complex thereby increasing receptor heterodimerization and in turn the signaling capability by IL-4 and IL-13. |
Databáze: | OpenAIRE |
Externí odkaz: |