Interleukin-1β increases leukemia inhibitory factor mRNA levels through transient stimulation of transcription rate

Christopher D. Carlson, Yuchen Bai, G. Miller Jonakait, Ronald P. Hart

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


Interleukin-1β (IL-1β) induces leukemia inhibitor factor (LIF) expression in a number of cell types including non-neuronal cells of the sympathetic superior cervical ganglion (SCG). Upregulation of LIF by inflammatory cytokines is usually associated with injury response. We characterized the molecular mechanism of LIF mRNA regulation by IL-1β in explanted neonatal rat SCG and a Schwann cell line. IL-1β increases LIF mRNA levels by interacting with IL-1 receptors in SCG, since this induction could be diminished by inclusion of either soluble IL-1 receptors or IL-1 receptor antagonist. The antiinflammatory glucocorticoid dexamethasone also inhibits LIF mRNA induction by IL-1β. LIF mRNA encodes a 3' AU-rich mRNA stability control sequence, but IL-1β does not appear to regulate the decay of LIF mRNA by this mechanism. IL-1β does not raise LIF gene transcription rate in cultured SCG 6 or 24 h after addition of IL-1β as measured by nuclear run- on assays. LIF gene transcription is induced rapidly and transiently in an immortalized Schwann cell line, returning to uninduced rates by 1 h after induction. These results suggest that the IL-1β induction of LIF gene expression is at least partially transcriptional, but that LIF mRNA increases to a greater extent than LIF transcription, suggesting the possibility of posttranscriptional regulation as well.

Original languageEnglish (US)
Pages (from-to)141-151
Number of pages11
Issue number2
StatePublished - Oct 1996

All Science Journal Classification (ASJC) codes

  • Neurology
  • Cellular and Molecular Neuroscience


  • Inflammation
  • Interleukin-1
  • Leukemia inhibitory factor
  • Posttranscriptional regulation
  • Schwann cells
  • Sympathetic ganglia
  • Transcription
  • mRNA stability


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