Alteration in survival signal induction by transient hypoxia in mice expressing mutant human SOD1 protein

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

Research output: Contribution to journalArticlepeer-review


Expression of survival phosphorylated serine/threonine kinase AKT (p-AKT) and phosphorylated extracellular signal-regulated kinase (p-ERK) signals was examined by immunohistochemistry and Western blotting in the lumbar spinal cord of 12-week-old mice with human mutant G93A Cu/Zn superoxide dismutase (SOD1) gene (Tg) and their wild-type (Wt) littermates during normoxia and 0 and 6 h after 2 h of 9% hypoxia. During nomoxia, a stronger p-AKT signal was detected in the nucleus of 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 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 returned to baseline level. 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)73-81
Number of pages9
JournalInternational Congress Series
Issue numberC
Publication statusPublished - Jun 1 2003


  • 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

  • General Medicine


Dive into the research topics of 'Alteration in survival signal induction by transient hypoxia in mice expressing mutant human SOD1 protein'. Together they form a unique fingerprint.

Cite this