Increased plasma lipid-poor apolipoprotein A-I in patients with coronary artery disease.
BACKGROUND
Pre-beta 1-HDL participates in a cyclic process involved in the retrieval of cholesterol from peripheral tissues. Although pre-beta 1-HDL can be measured by two-dimensional electrophoresis or crossed immunoelectrophoresis, these methods are time-consuming and require technical expertise. In this study, we separated plasma lipid-poor apolipoprotein A-I (apo A-I) by high-performance size-exclusion chromatography.


METHODS
We measured plasma lipid-poor apo A-I in 20 male patients with coronary artery disease [CAD; mean (SD) age, 64.0 (18) years] and 15 male controls [54.7 (17) years] and in 7 female CAD patients [70.3 (7.7) years] and 9 female controls [65.1 (4.7) years].


RESULTS
Lipid-poor apo A-I was most stable when stored at -80 degrees C in the presence of aprotinin (final concentration, 50 kIU/L). The lipid-poor apo A-I concentration decreased during incubation at 37 degrees C, and this was not prevented by the addition of 2 mmol/L of the lecithin:cholesterol acyltransferase (LCAT) inhibitor 5,5'-dithiobis(2-nitrobenzoic acid). Lipid-poor apo A-I was significantly higher in CAD patients than in controls [38.3 (7.9) mg/L for male CAD patients vs 29.3 (7.3) mg/L for male controls; 43.3 (11) mg/L for female CAD patients vs 27.1 (7.4) mg/L for female controls (P <0.01 for both)]. There were no significant differences in LCAT activity or cholesteryl ester transfer protein (CETP) concentration between patients and controls. Moreover, the plasma lipid-poor apo A-I concentration was not significantly correlated with LCAT or CETP activities.


CONCLUSIONS
Although the production of lipid-poor apo A-I in plasma is not fully understood, our results indicate that lipid-poor apo A-I could be used as a marker for arteriosclerosis and demonstrate that it is not identical to the pre-beta1-HDL measured by other methods.
Suzuki
Makiko
M
Department of Informative Clinical Medicine, Regeneration and Advanced Medical Science, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan.
Wada
Hisayasu
H
Maeda
Satoshi
S
Saito
Kuniaki
K
Minatoguchi
Shinya
S
Saito
Kazunori
K
Seishima
Mitsuru
M
D000368:Aged; D016632:Apolipoprotein A-I / Q000097:blood*; D002352:Carrier Proteins / Q000097:blood; D053480:Cholesterol Ester Transfer Proteins; D002850:Chromatography, Gel; D003324:Coronary Artery Disease / Q000097:blood*; D004228:Dithionitrobenzoic Acid / Q000494:pharmacology; D005260:Female; D006023:Glycoproteins / Q000097:blood; D053442:High-Density Lipoproteins, Pre-beta; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000037:antagonists & inhibitors; D010949:Plasma
D016632:Apolipoprotein A-I; C506642:CETP protein, human; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D006023:Glycoproteins; D053442:High-Density Lipoproteins, Pre-beta; D008075:Lipoproteins, HDL; D004228:Dithionitrobenzoic Acid; D007862:Phosphatidylcholine-Sterol O-Acyltransferase