Motheaten (me/me) mice deficient in SHP-1 are less susceptible to focal cerebral ischemia

Celine A. Beamer, Diane M. Brooks, Diana I. Lurie

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


We have demonstrated previously that the protein tyrosine phosphatase SHP-1 seems to play a role in glial development and is upregulated in non-dividing astrocytes after injury. The present study examines the effect of loss of SHP-1 on the CNS response to permanent focal ischemia. SHP-1 deficient (me/me) mice and wild-type littermates received a permanent middle cerebral artery occlusion (MCAO). At 1, 3, and 7 days after MCAO, infarct volume, neuronal survival and cell death, gliosis, and inflammatory cytokine levels were quantified. SHP-1 deficient me/me mice display smaller infarct volumes at 7 days post-MCAO, increased neuronal survival within the ischemic penumbra, and decreased numbers of cleaved caspase 3+ cells within the ischemic core compared with wild-type mice. In addition, me/me mice exhibit increases in GFAP+ reactive astrocytes, F4-80+ microglia, and a concomitant increase in the level of interleukin 12 (IL-12) over baseline compared with wild-type. Taken together, these results demonstrate that loss of SHP-1 results in greater healing of the infarct due to less apoptosis and more neuronal survival in the ischemic core and suggests that pharmacologic inactivation of SHP-1 may have potential therapeutic value in limiting CNS degeneration after ischemic stroke.

Original languageEnglish
Pages (from-to)1220-1230
Number of pages11
JournalJournal of Neuroscience Research
Issue number7
StatePublished - May 15 2006


  • Cytokine
  • Gliosis
  • Infarct volume
  • Ischemia
  • Motheaten
  • SHP-1


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