ADAMTS13 gene deletion aggravates ischemic brain damage: A possible neuroprotective role of ADAMTS13 by ameliorating postischemic hypoperfusion

  • Fujioka M
  • Hayakawa K
  • Mishima K
 et al. 
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Abstract

Reperfusion after brain ischemia causes thrombus formation and microcirculatory disturbances, which are dependent on the platelet glycoprotein Ib-von Willebrand factor (VWF) axis. Because ADAMTS13 cleaves VWF and limits platelet-dependent thrombus growth, ADAMTS13 may ameliorate ischemic brain damage in acute stroke. We investigated the effects of ADAMTS13 on ischemia-reperfusion injury using a 30-minute middle cerebral artery occlusion model in Adamts13(-/-) and wild-type mice. After reperfusion for 0.5 hours, the regional cerebral blood flow in the ischemic cortex was decreased markedly in Adamts13(-/-) mice compared with wild-type mice (P < .05), which also resulted in a larger infarct volume after 24 hours for Adamts13(-/-) compared with wild-type mice (P < .01). Thus, Adamts13 gene deletion aggravated ischemic brain damage, suggesting that ADAMTS13 may protect the brain from ischemia by regulating VWF-platelet interactions after reperfusion. These results indicate that ADAMTS13 may be a useful therapeutic agent for stroke.

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Authors

  • Masayuki Fujioka

  • Kazuhide Hayakawa

  • Kenichi Mishima

  • Ai Kunizawa

  • Keiichi Irie

  • Sei Higuchi

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