Protein co-expression with axonal injury in multiple sclerosis plaques
Protein co-expression with axonal injury in multiple sclerosis plaques
复制标题
DOI：
10.1007/s00401-006-0045-0
复制
发表时间：
2006-04-01
影响因子：
12.7
通讯作者：
Esiri, MM
中科院分区：
文献类型：
--
作者：
Diaz-Sanchez, M;Williams, K;Esiri, MM
急性多发性硬化（MS）病变中轴突的损伤现已得到充分证实，但这种损伤的机制仍不清楚。在这里，我们应用了一组抗体，这些抗体可以识别细胞群和其中所含的蛋白质，以检测那些在急性，亚急性和边缘活动性MS斑块中特别靠近受损轴突的细胞和蛋白质。结果以半定量的方式表达，生成的图表显示许多标记物在轴突损伤部位的表达增强。然而，与轴突损伤相关的表达的最急剧增加见于钙蛋白酶I（μ-钙蛋白酶）、诱导型一氧化氮合酶和MMP-2，表明这些蛋白质可能形成负责MS病变中所见的髓鞘和/或轴突损伤的起始的一组蛋白质的一部分。
Damage to axons in acute multiple sclerosis (MS) lesions is now well established but the mechanisms of this damage remain obscure. Here we have applied a panel of antibodies that identify cell populations and proteins contained in them with a view to detecting those cells and proteins that are localised particularly closely to damaged axons in acute, sub-acute and border-active MS plaques. Results are expressed semi-quantitatively and graphs produced that show that many of the markers show enhanced expression at sites of axon damage. However, the sharpest increase in expression in relation to axon damage was seen for Calpain I (mu-calpain), inducible nitric oxide synthase and MMP-2, suggesting that these proteins may form part of a group of proteins responsible for the initiation of myelin and/or axon damage seen in MS lesions.