Decay-accelerating factor in the cardiomyocytes of normal individuals and patients with myocardial infarction.
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.
Institute of Pathology, University of Bern, Switzerland.
A
A
Zimmermann
H
H
Gerber
V
V
Nussenzweig
H
H
Isliker
D000368:Aged; D000369:Aged, 80 and over; D018958:CD55 Antigens; D003169:Complement Inactivator Proteins / Q000032:analysis*; D005260:Female; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000032:analysis*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology*
D018958:CD55 Antigens; D003169:Complement Inactivator Proteins; D008565:Membrane Proteins