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

Guang Jin1, Takeshi Hayashi, Junichi Kawagoe

  • 1Department of Neurology, Graduate School of Medicine and Dentistry, Okayama University, Okayama, Japan.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|January 14, 2005
PubMed

Insights

Protease-activated receptor-2 (PAR-2) deficiency exacerbates ischemic stroke injury in mice. Loss of PAR-2 suppresses neuronal ERK activation and reactive astrocyte responses, increasing brain damage after stroke.

Area of Science:

  • Neuroscience
  • Cerebrovascular Research
  • Molecular Biology

Background:

  • Protease-activated receptor-2 (PAR-2) is implicated in various physiological and pathological processes.
  • Its role in acute ischemic stroke, particularly concerning neuronal signaling and glial responses, remains incompletely understood.

Purpose of the Study:

  • To investigate the expression profile of PAR-2 in the central nervous system (CNS) following transient middle cerebral artery occlusion (tMCAO).
  • To determine the impact of PAR-2 gene knockout (PAR-2 KO) on infarct size, neuronal activation, and astrocyte response after ischemic stroke.

Main Methods:

  • Transient middle cerebral artery occlusion (tMCAO) model in mice.
  • Analysis of PAR-2 expression, infarct volume, TUNEL staining, phosphorylated extracellular signal-regulated kinase (p-ERK) levels, and astroglial activation.
  • Comparison between wild-type and PAR-2 KO mice.

Main Results:

  • PAR-2 is expressed in CNS neurons and upregulated post-tMCAO.
  • PAR-2 deficiency significantly increased infarct volume and cell death (TUNEL-positive cells).
  • Neuronal p-ERK activation and reactive astroglial activation were suppressed in PAR-2 KO mice.

Conclusions:

  • PAR-2 deficiency worsens acute ischemic cerebral injury.
  • The protective effects of PAR-2 may involve the modulation of neuronal ERK signaling and reactive astroglial activation.

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