LIF-mediated activation of STAT proteins after neuronal injury in vivo

Neuroreport. 1995 Nov 13;6(16):2240-4. doi: 10.1097/00001756-199511000-00033.

Abstract

Leukemia inhibitory factor (LIF) is a member of a family of neuropoietic cytokines which influence neuronal survival, differentiation and response to injury. In cell lines LIF activates the Jak/Tyk tyrosine kinases and the STAT family of transcription factors. We have investigated whether the Jak-STAT intracellular signaling pathway is activated by LIF after neuronal injury in vivo. Axotomy of postganglionic sympathetic nerves resulted in sustained activation of members of the STAT transcription factor family. This activation is dependent on LIF as axotomy failed to activate STAT proteins in LIF-deficient mice. These data indicate that LIF-dependent activation of STAT proteins is one of the signal transduction pathways activated after neuronal injury.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Axons / physiology*
  • Gene Expression
  • Growth Inhibitors / deficiency
  • Growth Inhibitors / physiology*
  • Interleukin-6*
  • Leukemia Inhibitory Factor
  • Lymphokines / deficiency
  • Lymphokines / physiology*
  • Male
  • Mice
  • Mice, Mutant Strains
  • Neurons / drug effects*
  • Neurons / ultrastructure
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction / physiology*
  • Superior Cervical Ganglion / physiology*
  • Sympathectomy
  • Sympathetic Fibers, Postganglionic / physiology
  • Trans-Activators*
  • Vasoactive Intestinal Peptide / genetics

Substances

  • Growth Inhibitors
  • Interleukin-6
  • Leukemia Inhibitory Factor
  • Lif protein, mouse
  • Lymphokines
  • Trans-Activators
  • Vasoactive Intestinal Peptide