BLOOD CARDIOLIPIN IN HEMODIALYSIS-PATIENTS, ITS IMPLICATION IN THE BIOLOGICAL ACTION OF PLATELET-ACTIVATING-FACTOR

Citation
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
Citations number
32
Categorie Soggetti
Biology,"Cell Biology
ISSN journal
13572725
Volume
28
Issue
1
Year of publication
1996
Pages
43 - 51
Database
ISI
SICI code
1357-2725(1996)28:1<43:BCIHII>2.0.ZU;2-E
Abstract
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.