Deficiency of PAR-2 gene increases acute focal ischemic brain injury

Guang Jin, Takeshi Hayashi, Junichi Kawagoe, Toshiaki Takizawa, Tetsuya Nagata, Isao Nagano, Mikio Syoji, Koji Abe

Research output: Contribution to journalArticlepeer-review

41 Citations (Scopus)


The expression profile of the protease-activated receptor-2 (PAR-2) and effects of PAR-2 gene knockout (PAR-2 KO) on the infarct size were investigated after 60 minutes of transient middle cerebral artery occlusion (tMCAO) in mice in relation to phosphorylated extracellular signal-regulated kinase (p-ERK) and astrocyte activation. PAR-2 was normally distributed mainly in neurons of the central nervous system (CNS), and strongly upregulated at 8-24 hours after tMCAO. Deficiency of PAR-2 gene significantly increased the infarct volume and the number of TUNEL-positive cells at 24 hours of reperfusion. The strong neuronal expression of p-ERK was induced at 5 minutes as a peak after reperfusion in wild-type mice, but the signal change was significantly reduced in PAR-2 KO mice. Astroglial activation was also greatly inhibited at 24 hours after tMCAO in PAR-2 KO mice. These results show that the deficiency of PAR-2 gene increases the acute ischemic cerebral injury associating with suppression of neuronal ERK activation and reactive astroglial activation.

Original languageEnglish
Pages (from-to)302-313
Number of pages12
JournalJournal of Cerebral Blood Flow and Metabolism
Issue number3
Publication statusPublished - Mar 2005
Externally publishedYes


  • ERK
  • GFAP
  • Ischemia
  • Knockout mice
  • NeuN
  • PAR-2

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine


Dive into the research topics of 'Deficiency of PAR-2 gene increases acute focal ischemic brain injury'. Together they form a unique fingerprint.

Cite this