Reduced cortical injury and edema in tissue plasminogen activator knockout mice after brain trauma

被引:37
作者
Mori, T
Wang, XY
Kline, AE
Siao, CJ
Dixon, CE
Tsirka, SE
Lo, EH
机构
[1] Massachusetts Gen Hosp, Neuroprotect Res Lab, Charlestown, MA 02129 USA
[2] Harvard Univ, Sch Med, Program Neurosci, Charlestown, MA 02129 USA
[3] Univ Pittsburgh, Dept Neurol Surg, Brain Trauma Res Ctr, Pittsburgh, PA 15260 USA
[4] SUNY Stony Brook, Dept Pharmacol, Stony Brook, NY 11794 USA
关键词
blood-brain barrier; brain edema; extracellular matrix; neuroprotection; proteolysis;
D O I
10.1097/00001756-200112210-00051
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Tissue plasminogen activator (tPA) may play a deleterious role after brain injury. Here, we compared the response to traumatic brain injury in tPA knockout (KO) and wildtype (WT) mice after controlled cortical impact. At 6 h after trauma, blood-brain barrier permeability was equally increased in all mice. However, by 24 h specific gravity measurements of brain edema were significantly worse in WT mice than in KO mice. At 1 and 2 days post-trauma, mice showed deficits in rotarod performance, but by day 7 all mice recovered motor function and there were no differences between WT and KO mice. At 7 days, cortical lesion volumes were significantly reduced in KO mice compared with WT mice. However, there were no significant differences: in CA3 hippocampal neuron survival. These data suggest that tPA amplifies cortical brain damage and edema in this mouse model of traumatic brain injury. NeuroReport 12:4117-4120 (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:4117 / 4120
页数:4
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