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J Biol Chem, Vol. 275, Issue 6, 3841-3847, February 11, 2000
From the During catabolic diseases such as sepsis,
inflammation, and infection, a state of growth hormone (GH) resistance
develops in liver. This has been attributed in part to increased
production of the proinflammatory cytokine interleukin-1
Role of the Suppressor of Cytokine Signaling-3 in Mediating the
Inhibitory Effects of Interleukin-1
on the Growth
Hormone-dependent Transcription of the Acid-labile
Subunit Gene in Liver Cells*
§,,,, and Department of Animal Science, Cornell
University, Ithaca, New York 14853 and ¶ Prince Henry's
Institute of Medical Research, Clayton, Victoria 3168, Australia
(IL-1).
To determine how IL-1 induces GH resistance, we studied the
acid-labile subunit (ALS) gene whose hepatic transcription is increased
by GH via the Janus kinase-signal transducer and activator of
transcription (JAK-STAT) pathway. IL-1 reduced the ability of GH to
stimulate ALS mRNA in rat primary hepatocytes and ALS promoter
activity in H4-II-E rat hepatoma cells. This inhibition was dependent
on ALSGAS1, an element resembling a 
-interferon activated sequence that mediates the transcriptional effects of GH. Inhibition by IL-1
was also associated with a reduction of GH-dependent
binding of STAT5 to this element after chronic (8 and 24 h), but
not after acute treatment (15 min). Because these results indicated
that the inhibition by IL-1 was indirect, expression of the recently discovered suppressors of cytokine action (SOCS) was examined in liver
cells. IL-1 did not alter the expression of SOCS1, SOCS2, and CIS,
indicating that they are not involved. In contrast, IL-1 increased
SOCS3 mRNA by 8-fold after 24 h of treatment, whereas GH had
no effect. Forced expression of SOCS3 was just as effective as IL-1
in reducing the GH induction of ALS promoter activity in H4-II-E rat
hepatoma cells. Similar results were observed in primary rat
hepatocytes. We conclude that the induction of SOCS3 by IL-1
contributes to the development of GH resistance in liver, and
represents a mechanism by which cytokines such as IL-1 cross-talk with cytokines using the JAK-STAT pathway.
*
This work was supported by National Institutes of Health
Grant DK-51624 (to Y. R. B.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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