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RESEARCH PRODUCT
Oncostatin M, leukaemia-inhibitory factor and interleukin 6 trigger different effects on alpha1-proteinase inhibitor synthesis in human lung-derived epithelial cells.
James TravisStefan Rose JohnJoanna Cichysubject
medicine.medical_specialtyendocrine systemProtein subunitBlotting WesternOncostatin MInhibitory postsynaptic potentialBiochemistryLeukemia Inhibitory FactorInternal medicinemedicineTumor Cells CulturedHumansInterleukin 6ReceptorMolecular BiologyLungLymphokinesbiologyChemistryInterleukin-6fungiOncostatin MOncostatin M receptorEpithelial CellsCell BiologyGlycoprotein 130Blotting NorthernGrowth InhibitorsCell biologyInterleukin 31Endocrinologyalpha 1-Antitrypsinbiology.proteinPeptidesResearch Articledescription
Interleukin 6 (IL-6), oncostatin M (OSM) and leukaemia-inhibitory factor (LIF) share a common signal-transducing subunit in each of their receptors and thus mediate an overlapping spectrum of biological activities. Although all of these cytokines stimulate the production of α1-proteinase inhibitor (α1-PI) in hepatocyte-derived cells, only OSM is able to up-regulate levels of this inhibitor in epithelial cells originating from the lung. In this study we characterized human lung-derived epithelial-like HTB58 cells for their ability to synthesize α1-PI after treatment with IL-6, OSM and LIF. The results demonstrate that the resistance of HTB58 cells to the effects of IL-6 and LIF was not because of a lack of their individual functional receptors and suggest that OSM utilizes two different receptors, gp130/LIF receptor and gp130/OSM receptor, in lung-derived epithelial cells.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1998-01-15 | The Biochemical journal |