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Activation systems for latent matrix metalloproteinase-2 are upregulated immediately after focal cerebral ischemia

Dae-Il Chang1, Naohisa Hosomi, Jacinta Lucero

  • 1Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|December 10, 2003
PubMed

Insights

Matrix metalloproteinase-2 (MMP-2) activation in the brain

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Matrix metalloproteinase-2 (MMP-2) degrades basal lamina, compromising microvessel integrity during focal cerebral ischemia.
  • MMP-2 is secreted as a latent proenzyme (pro-MMP-2), and its activation mechanism in ischemic brain regions remains unclear.

Purpose of the Study:

  • To investigate the expression and activation of MMP-2 and its activators in the primate brain following focal cerebral ischemia.
  • To elucidate the early molecular events contributing to microvascular damage in ischemic stroke.

Main Methods:

  • Immunohistochemistry and in situ hybridization were used to examine the expression of MMP-2, MT1-MMP, MT3-MMP, urokinase (u-PA), its receptor (u-PAR), and plasminogen activator inhibitor-1 (PAI-1).
  • Samples were obtained from the basal ganglia of adolescent male baboons subjected to middle cerebral artery occlusion/reperfusion.

Main Results:

  • Expressions of MMP-2, MT1-MMP, MT3-MMP, u-PA, u-PAR, and PAI-1 were significantly increased within 1 hour in the ischemic core after middle cerebral artery occlusion.
  • mRNA transcripts confirmed early increases in latent MMP-2, u-PA, u-PAR, and PAI-1.
  • Tissue plasminogen activator expression did not increase.

Conclusions:

  • The findings suggest rapid secretion of pro-MMP-2 and its activators in the ischemic primate striatum.
  • The coordinated early appearance of pro-MMP-2 and its activation system indicates its potential role in matrix degradation and microvascular injury during focal cerebral ischemia.

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