Sustained induction of survival p-AKT and p-ERK signals after transient hypoxia in mice spinal cord with G93A mutant human SOD1 protein

Hristelina Ilieva, Isao Nagano, Tetsuro Murakami, Mito Shiote, Mikio Shoji, Koji Abe

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Expression of survival p-AKT and p-ERK signals was examined by immunohistochemistry and Western blotting in the lumbar spinal cord of 12-week-old presymptomatic mice with human mutant G93A SOD1 gene (transgenic, Tg) and their wild-type (Wt) littermates during normoxia, and 0 and 6 h after 2 h of 9% hypoxia. During normoxia, a stronger p-AKT signal was detected in the nucleus of the motor neurons of Tg animals. At 0 h of recovery from 2 h of hypoxia, both p-AKT and p-ERK signals were induced at a slightly lower level in Tg (1.1-1.2-fold) compared to those of Wt (1.2-1.5-fold) animals. At 6 h of recovery, both p-AKT and p-ERK signals were sustained in the lumbar spinal motor neurons of Tg animals, while those in Wt animals quickly returned to baseline level. As a control, at 6 h of recovery, the hippocampus of Tg animals showed significantly sustained p-AKT levels, but not p-ERK levels, compared to Wt. The current results suggest that the presence of mutant SOD1 alters survival p-AKT and p-ERK signals, possibly to compensate for the acquired gain-of-function of the mutant protein.

Original languageEnglish
Pages (from-to)57-62
Number of pages6
JournalJournal of the neurological sciences
Volume215
Issue number1-2
DOIs
Publication statusPublished - Nov 15 2003

Keywords

  • Amyotrophic lateral sclerosis (ALS)
  • Hypoxia
  • Phosphorylated extracellular signal-regulated kinase (p-ERK)
  • Phosphorylated serine/ threonine kinase AKT (p-AKT)
  • Superoxide dismutase 1 (SOD1)

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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