Diaz-Sanchez Maria, Williams Kelly, DeLuca Gabriele C, Esiri Margaret M
Department of Clinical Neurology, University of Oxford, Radcliffe Infirmary, OX2 6HE, Oxford, UK.
Acta Neuropathol. 2006 Apr;111(4):289-99. doi: 10.1007/s00401-006-0045-0. Epub 2006 Mar 18.
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 (micro-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.
急性多发性硬化症（MS）病灶中的轴突损伤现已得到充分证实，但其损伤机制仍不清楚。在此，我们应用了一组抗体，这些抗体可识别细胞群体及其所含蛋白质，旨在检测那些在急性、亚急性和边缘活动性MS斑块中特别紧密定位于受损轴突的细胞和蛋白质。结果以半定量方式表示，并绘制了图表，结果表明许多标志物在轴突损伤部位表达增强。然而，与轴突损伤相关的表达增加最为明显的是钙蛋白酶I（微钙蛋白酶）、诱导型一氧化氮合酶和基质金属蛋白酶-2，这表明这些蛋白质可能是导致MS病灶中髓鞘和/或轴突损伤起始的一组蛋白质的一部分。
