ERK 1/2 signaling pathway is involved in nicotine-mediated neuroprotection in spinal cord neurons

Michal Toborek, Kwang Won Son, Anna Pudelko, Kelley King-Pospisil, Edward Wylegala, Andrzej Malecki

Research output: Contribution to journalArticle

42 Scopus citations

Abstract

Evidence indicates that agonists of neuronal nicotinic receptors (nAChRs), including nicotine, can induce neuroprotective and anti-apoptotic effects in the CNS. To study these mechanisms, the present study focused on nicotine-mediated modulation of the extracellular regulated kinase 1 and 2 (ERK1/2) pathway in cultured spinal cord neurons. Exposure to nicotine (0.1-10 μM) for as short as 1 min markedly upregulated levels of phosphorylated ERK1/2 (pERK1/2) and increased total ERK1/2 activity. Inhibition studies with mecamylamine and α-bungarotoxin revealed that these effects were mediated by the α7 nicotinic receptor. In addition, pre-exposure to U0126, a specific inhibitor of the ERK1/2 signaling, prevented nicotine-mediated anti-apoptotic effects. To indicate if treatment with nicotine also can activate ERK1/2 in vivo, a moderate spinal cord injury (SCI) was induced in rats using a weight-drop device and nicotine was injected 2 h post-trauma. Consistent with in vitro data, nicotine increased levels of pERK1/2 in this animal model of spinal cord trauma. Results of the present study indicate that the ERK1/2 pathway is involved in anti-apoptotic effects of nicotine in spinal cord neurons and may be involved in therapeutic effects of nicotine in spinal cord trauma.

Original languageEnglish (US)
Pages (from-to)279-292
Number of pages14
JournalJournal of cellular biochemistry
Volume100
Issue number2
DOIs
StatePublished - Feb 1 2007
Externally publishedYes

Keywords

  • Apoptosis
  • Fatty acids
  • Nicotine
  • Signal transduction
  • Spinal cord injury

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

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