Expression of PTEN and its phosphorylated form after transient middle cerebral artery occlusion in rat

N. Omori, G. Jin, F. Li, W. R. Zhang, S. J. Wang, Y. Hamakawa, I. Nagano, Y. Manabe, M. Shoji, K. Abe

Research output: Contribution to journalArticlepeer-review


A phosphatase PTEN (phosphatase and tensin homologue deleted on chromosome 10) is a tumor suppressor gene that suppresses cell growth, inhibits cell migration, and induces apoptosis. The phosphorylated form of PTEN (p-PTEN) is a key survival factor relating PI3K-Akt pathway and their downstream effectors. Spatiotemporal profiles of PTEN and p-PTEN expression were immunohistochemically examined after 90 min of transient middle cerebral artery occlusion in rats. In the ischemic core, PTEN progressively decreased by 3 days, whereas a rapid but transient increase of p-PTEN was found with a peak at 1 h after the reperfusion. In contrast, in the ischemic penumbra, PTEN showed a minor change and a gradual but sustained p-PTEN expression was observed in the ischemic penumbra with a peak at 12 h. In addition, the balance of population among strongly, moderately, and weakly stained cells was different between the ischemic core and penumbra at their peak time points. These results suggest an important role of p-PTEN for cell survival after ischemia as an upstream regulator for PI3K-Akt.

Original languageEnglish
Pages (from-to)3-11
Number of pages9
JournalInternational Congress Series
Issue numberC
Publication statusPublished - Jun 1 2003
Externally publishedYes


  • Akt
  • Apoptosis
  • MCAO
  • PI3K
  • PTEN
  • Phospho-PTEN

ASJC Scopus subject areas

  • General Medicine


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