S. Antonopoulou et al., BLOOD CARDIOLIPIN IN HEMODIALYSIS-PATIENTS, ITS IMPLICATION IN THE BIOLOGICAL ACTION OF PLATELET-ACTIVATING-FACTOR, International journal of biochemistry & cell biology, 28(1), 1996, pp. 43-51
Bovine heart cardiolipin specifically inhibits rabbit platelet aggrega
tion induced by PAF in vitro. Tn the past we have reported that patien
ts with primary glomerulonephritis have increased PAF levels in plasma
(Iatrou et al., 1995b). In this work we investigate the existence of
cardiolipin in the blood of end-stage renal patients due to primary gl
omerulonephritis and we study its implication in the biological study
of PAF. Lipids from blood samples of end-stage renal patients were ext
racted, fractionated onto silicic acid column and onto High Performanc
e Liquid Chromatography (HPLC) cation exchange column. PAF fraction wa
s removed and phospholipids were separated from the rest lipid fractio
n with current counter distribution and furthermore fractionated onto
HPLC silica column. The results show: 1. cardiolipin is present in the
blood of end-stage renal patients. 2. Blood cardiolipin specifically
inhibits PAF-induced aggregation in washed rabbit platelets, 3. Scatch
ard plot analysis of PAF binding, in the presence of unlabelled PAF an
d in the presence of cardiolipin, shows that rabbit platelets possess
two different types of binding sites. One of which is saturable and of
high affinity, kD = 0.103 +/- 0.03 nM (SEM, n = 3) with 337 +/- 94 bi
nding sites per platelet for PAF and kD = 0.087 +/- 0.02 nM with 371 /- 92.7 binding sites per platelet for cardiolipin while the other one
has almost infinite binding capacity. 4. Blood cardiolipin competes [
H-3]PAF binding in rabbit platelets. This work shows that cardiolipin
exists in the blood of end-stage renal patients and specifically inhib
its PAF-induced aggregation as well as PAF binding in rabbit platelets
. The possible implication of the biological actions of cardiolipin in
the anticardiolipin-antiphospholipid syndrome is also discussed.