ADAMTS13 gene deletion aggravates ischemic brain damage: a possible neuroprotective role of ADAMTS13 by ameliorating postischemic hypoperfusion
Copyright policy )ADAMTS13 gene deletion aggravates ischemic brain damage: a possible neuroprotective role of ADAMTS13 by ameliorating postischemic hypoperfusion
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.
- TU Dresden Germany
- Fukuoka University Japan
- Fukuoka University Japan
- Nara Medical University Japan
- National Cerebral and Cardiovascular Center Japan
Mice, Knockout, Time Factors, ADAMTS13 Protein, Metalloendopeptidases, Brain Ischemia, Stroke, Mice, Neuroprotective Agents, Cerebrovascular Circulation, Reperfusion Injury, von Willebrand Factor, Animals, Gene Deletion
Mice, Knockout, Time Factors, ADAMTS13 Protein, Metalloendopeptidases, Brain Ischemia, Stroke, Mice, Neuroprotective Agents, Cerebrovascular Circulation, Reperfusion Injury, von Willebrand Factor, Animals, Gene Deletion
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