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RESEARCH PRODUCT
Regulation of the type II oncostatin M receptor expression in lung-derived epithelial cells
Ellen PuréStefan Rose JohnJoanna CichyJoanna Cichysubject
Cell typemedicine.medical_treatmentTransforming growth factor β1Respiratory SystemBronchial epitheliumBiophysicsBronchiOncostatin MInterleukin 1 receptor type IILeukemia Inhibitory FactorBiochemistryDexamethasoneAntigens CDStructural BiologyCytokine Receptor gp130GeneticsmedicineHumansReceptors CytokineReceptorLungMolecular BiologyLymphokinesMembrane GlycoproteinsbiologyInterleukin-6ChemistryfungiOncostatin MOncostatin M receptorEpithelial CellsReceptors Oncostatin MCell BiologyGrowth InhibitorsCell biologyInterleukin 31CytokineGene Expression Regulationbiology.proteinCancer researchCytokinesInflammation MediatorsPeptidesLeukemia inhibitory factordescription
AbstractOncostatin M (OSM) is a potent modulator of human lung-derived epithelial cell function. This cytokine binds two distinct receptor complexes: type I OSM receptor which is also a functional receptor for leukemia inhibitory factor (LIF), and type II OSM-specific receptor. The role of these two distinct receptors in mediating the response of individual cell types to OSM has not been delineated. In contrast to LIF, OSM induces synthesis of α1-antichymotrypsin and α1-antiproteinase inhibitor in lung-derived epithelial cells. The differential responsiveness to LIF and OSM suggested that the response of lung epithelial cells to OSM may be mediated by the OSM-specific receptor. Therefore, we characterized lung-derived epithelial cells for the expression of type II OSM receptor mRNAs, and the regulation of the mRNAs encoding the components of the OSM-specific receptor by cytokines and dexamethasone.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1998-07-14 | FEBS Letters |