ONCOSTATIN-M, LEUKEMIA-INHIBITORY FACTOR AND INTERLEUKIN-6 TRIGGER DIFFERENT EFFECTS ON ALPHA(1)-PROTEINASE INHIBITOR SYNTHESIS IN HUMAN LUNG-DERIVED EPITHELIAL-CELLS

Citation
J. Cichy et al., ONCOSTATIN-M, LEUKEMIA-INHIBITORY FACTOR AND INTERLEUKIN-6 TRIGGER DIFFERENT EFFECTS ON ALPHA(1)-PROTEINASE INHIBITOR SYNTHESIS IN HUMAN LUNG-DERIVED EPITHELIAL-CELLS, Biochemical journal, 329, 1998, pp. 335-339
Citations number
26
Categorie Soggetti
Biology
Journal title
ISSN journal
02646021
Volume
329
Year of publication
1998
Part
2
Pages
335 - 339
Database
ISI
SICI code
0264-6021(1998)329:<335:OLFAIT>2.0.ZU;2-V
Abstract
Interleukin 6 (IL-6), oncostatin M (OSM) and leukaemia-inhibitory fact or (LIF) share a common signal-transducing subunit in each of their re ceptors and thus mediate an overlapping spectrum of biological activit ies. Although all of these cytokines stimulate the production of alpha (1)-proteinase inhibitor (alpha(1)-PI) in hepatocyte-derived cells, on ly OSM is able to up-regulate levels of this inhibitor in epithelial c ells originating from the lung. In this study we characterized human l ung-derived epithelial-like HTB58 cells for their ability to synthesiz e alpha(1)-PI after treatment with IL-6, OSM and LIF. The results demo nstrate 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 rece ptor and gp130/OSM receptor, in lung-derived epithelial cells.