Vougioukas V I, Roeske S, Michel U, Brück W
Department of Neuropathology, University of Göttingen, Germany.
Am J Pathol. 1998 Jan;152(1):241-9.
Wallerian degeneration of the peripheral nervous system was studied in ICAM-1-deficient mice and compared with the phenomena observed in C57BL wild-type animals. There was a decrease in myelin density in both mice strains 4 and 6 days after transection of the sciatic nerve. The degenerating nerves were invaded by Mac-1-, LFA-1-, and F4/80-positive macrophages; significantly lower numbers of macrophages were present in ICAM-1-deficient nerves. Myelin loss decreased after nerve transection with a more prominent loss in ICAM-1-deficient animals. Schwann cells revealed a much higher myelin load in these animals when compared with wild-type nerves, and there was an increased proliferation of endoneurial cells in ICAM-1-deficient mice. These data indicate that ICAM-1 is involved in macrophage recruitment to injured peripheral nerves as well as in the proliferative and phagocytic response of Schwann cells after peripheral nerve transection.
在ICAM-1缺陷小鼠中研究了周围神经系统的沃勒变性,并与在C57BL野生型动物中观察到的现象进行了比较。在坐骨神经横断后第4天和第6天,两种小鼠品系的髓磷脂密度均降低。变性神经被Mac-1、LFA-1和F4/80阳性巨噬细胞侵入;ICAM-1缺陷神经中的巨噬细胞数量明显减少。神经横断后髓磷脂损失减少,ICAM-1缺陷动物中的损失更为明显。与野生型神经相比,这些动物的雪旺细胞显示出更高的髓磷脂负载,并且ICAM-1缺陷小鼠的神经内膜细胞增殖增加。这些数据表明,ICAM-1参与巨噬细胞向受损周围神经的募集,以及周围神经横断后雪旺细胞的增殖和吞噬反应。