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IL-1beta promotes neurite outgrowth by deactivating RhoA via p38 MAPK pathway.

AbstractExpression of the pro-inflammatory cytokine interleukin-1 beta (IL-1beta) is increased following the nervous system injury. Generally IL-1beta induces inflammation, leading to neural degeneration, while several neuropoietic effects have also been reported. Although neurite outgrowth is an important step in nerve regeneration, whether IL-1beta takes advantages on it is unclear. Now we examine how it affects neurite outgrowth. Following sciatic nerve injury, expression of IL-1beta is increased in Schwann cells around the site of injury, peaking 1 day after injury. In dorsal root ganglion (DRG) neurons and cerebellar granule neurons (CGNs), neurite outgrowth is inhibited by the addition of myelin-associated glycoprotein (MAG), activating RhoA. IL-1beta overcomes MAG-induced neurite outgrowth inhibition, by deactivating RhoA. Intracellular signaling experiments reveal that p38 MAPK, and not nuclear factor-kappa B (NF-kappaB), mediated this effect. These findings suggest that IL-1beta may contribute to nerve regeneration by promoting neurite outgrowth following nerve injury.
AuthorsKo Temporin, Hiroyuki Tanaka, Yusuke Kuroda, Kiyoshi Okada, Koji Yachi, Hisao Moritomo, Tsuyoshi Murase, Hideki Yoshikawa (Affiliation: Department of Orthopaedics, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.)
JournalBiochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 365 Issue 2 Pg. 375-80 (Jan 11 2008) ISSN: 1090-2104 United States
PMID17996195 (Publication Type: Journal Article)
Chemical References
  • Interleukin-1beta
  • p38 Mitogen-Activated Protein Kinases
  • rhoA GTP-Binding Protein
Topics
  • Animals
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Enzyme Activation (drug effects)
  • Female
  • Interleukin-1beta (administration & dosage)
  • MAP Kinase Signaling System (physiology)
  • Nerve Regeneration (drug effects, physiology)
  • Neurites (drug effects, physiology, ultrastructure)
  • Posterior Horn Cells (cytology, drug effects, physiology)
  • Rats
  • Rats, Wistar
  • p38 Mitogen-Activated Protein Kinases (metabolism)
  • rhoA GTP-Binding Protein (metabolism)