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