Zimmermann A, Gerber H, Nussenzweig V, Isliker H
Institute of Pathology, University of Bern, Switzerland.
Virchows Arch A Pathol Anat Histopathol. 1990;417(4):299-304. doi: 10.1007/BF01605780.
The presence of decay-accelerating factor (DAF) was clearly demonstrated on the surface of normal cardiomyocytes. In patients who had died of myocardial infarction (MI) cardiomyocytes displayed different appearances: outside the ischaemically damaged region the myocytes showed no significant variations in DAF expression when compared with controls without MI. Within myocardial zones damaged by ischaemia, however, apparently normal myocytes showed large gaps in surface staining of DAF or formed clusters which were entirely devoid of reactivity with anti-DAF antibodies. The number of DAF-deficient myocytes increased with the extent of necrosis and also with the number of days between onset of MI and death. Even though injury to myocytes is to a large extent related to anoxia and to the presence of free oxygen radicals, the complement system also appears to be involved; DAF may have protective functions against complement-mediated injury. We speculate that phospholipase may be involved in the removal of DAF from the cardiomyocyte surface.
在正常心肌细胞表面清晰显示出衰变加速因子（DAF）的存在。死于心肌梗死（MI）的患者的心肌细胞呈现出不同的外观：在缺血损伤区域之外，与无MI的对照组相比，心肌细胞的DAF表达没有显著差异。然而，在缺血损伤的心肌区域内，看似正常的心肌细胞在DAF表面染色上出现大的间隙或形成完全不与抗DAF抗体发生反应的簇。缺乏DAF的心肌细胞数量随着坏死程度以及MI发作至死亡之间的天数增加而增加。尽管心肌细胞损伤在很大程度上与缺氧和游离氧自由基的存在有关，但补体系统似乎也参与其中；DAF可能具有针对补体介导损伤的保护功能。我们推测磷脂酶可能参与从心肌细胞表面去除DAF。
