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Detection of a Soluble Form of the Complement Membrane Attack Complex Inhibitor CD59 in Plasma after Acute Myocardial Infarction
Author(s) -
Väkevä A.,
Lehto T.,
Takala A.,
Meri S.
Publication year - 2000
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.2000.00783.x
Subject(s) - myocardial infarction , cd59 , complement membrane attack complex , complement (music) , medicine , cardiology , complement system , chemistry , immunology , antibody , biochemistry , complementation , gene , phenotype
Activation of the complement system has been documented in both experimental and clinical studies of acute myocardial infarction (AMI). Our earlier immunohistochemical studies have shown that the deposition of the membrane attack complex (MAC) of complement is associated with the loss of protectin (CD59), a glycosyl‐phosphatidylinositol (GPI)‐anchored sarcolemmal regulator of MAC, from the human and rat infarcted myocardium. In this study we detected, using an enzyme immunoassay (EIA), CD59 in the plasma of AMI patients at a concentration of 23.0 ± 8.4 ng/ml (mean ± SD; n = 17) at 4 h and 27.3 ± 11.8 ng/ml ( n = 24) at 24 h after AMI. Both values were significantly higher than in healthy controls (7.8 ± 6.4 ng/ml; n = 20; P < 0.001). The amount of CD59 correlated with the level of soluble terminal complement complexes (SC5b‐9; r = 0.84; P < 0.01) in the plasmas of AMI patients. Our results suggest that myocardial damage leads to release of CD59 from the sarcolemmal cell membranes during AMI.