White matter injury due to experimental chronic cerebral hypoperfusion is associated with C5 deposition.
White matter injury due to experimental chronic cerebral hypoperfusion is associated with C5 deposition.
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DOI：
10.1371/journal.pone.0084802
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Mack WJ
中科院分区：
文献类型：
--
作者：
Liu Q;He S;Groysman L;Shaked D;Russin J;Scotton TC;Cen S;Mack WJ
C5 补体蛋白是一种有效的炎症介质，与中风和神经退行性疾病的发病机制有关。微血管衰竭被认为是一种潜在的损伤机制。沿着这些思路，本研究探讨了 C5 在慢性脑灌注不足的情况下的作用。实验性双侧颈动脉狭窄后，胼胝体中的 C5 蛋白沉积在 30 天内增加（p<0.05）。时间进程在时间上与白质损伤的出现一致。同时，双侧颈动脉狭窄小鼠和假手术小鼠的全身血清 C5 水平似乎没有差异，这表明存在局部脑过程。双侧颈动脉狭窄后，与 C5 充足的对照相比，C5 缺陷小鼠的胼胝体白质缺血减少（p<0.05）。此外，C5 缺陷小鼠表现出较少的反应性星形胶质细胞和小胶质细胞 (p<0.01)。这项研究表明，在慢性脑灌注不足的情况下，C5 补体蛋白可能在通过炎症介导白质损伤中发挥关键作用。
The C5 complement protein is a potent inflammatory mediator that has been implicated in the pathogenesis of both stroke and neurodegenerative disease. Microvascular failure is proposed as a potential mechanism of injury. Along these lines, this investigation examines the role of C5 in the setting of chronic cerebral hypoperfusion. Following experimental bilateral carotid artery stenosis, C5 protein deposition increases in the corpus callosum over thirty days (p<0.05). The time course is temporally consistent with the appearance of white matter injury. Concurrently, systemic serum C5 levels do not appear to differ between bilateral carotid artery stenosis and sham-operated mice, implicating a local cerebral process. Following bilateral carotid artery stenosis, C5 deficient mice demonstrate decreased white matter ischemia in the corpus callosum when compared to C5 sufficient controls (p<0.05). Further, the C5 deficient mice exhibit fewer reactive astrocytes and microglia (p<0.01). This study reveals that the C5 complement protein may play a critical role in mediating white matter injury through inflammation in the setting of chronic cerebral hypoperfusion.
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