Increased plasma lipid-poor apolipoprotein A-I in patients with coronary artery disease

Makiko Suzuki, Hisayasu Wada, Satoshi Maeda, Kuniaki Saito, Shinya Minatoguchi, Kazunori Saito, Mitsuru Seishima

Research output: Contribution to journalArticle

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Abstract

Background: Pre-β1-HDL participates in a cyclic process involved in the retrieval of cholesterol from peripheral tissues. Although pre-β1-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 °C in the presence of aprotinin (final concentration, 50 kIU/L). The lipid-poor apo A-I concentration decreased during incubation at 37 °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-β1-HDL measured by other methods.

Original languageEnglish
Pages (from-to)132-137
Number of pages6
JournalClinical Chemistry
Volume51
Issue number1
DOIs
Publication statusPublished - 01-01-2005
Externally publishedYes

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Apolipoprotein A-I
Coronary Artery Disease
Lipids
Plasmas
Computer aided design
Cholesterol Ester Transfer Proteins
Phosphatidylcholine-Sterol O-Acyltransferase
Two-Dimensional Immunoelectrophoresis
Nitrobenzoates
Anticholesteremic Agents
Professional Competence
Aprotinin
Size exclusion chromatography
Arteriosclerosis
Electrophoresis
Gel Chromatography
Cholesterol
Tissue

All Science Journal Classification (ASJC) codes

  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

Suzuki, Makiko ; Wada, Hisayasu ; Maeda, Satoshi ; Saito, Kuniaki ; Minatoguchi, Shinya ; Saito, Kazunori ; Seishima, Mitsuru. / Increased plasma lipid-poor apolipoprotein A-I in patients with coronary artery disease. In: Clinical Chemistry. 2005 ; Vol. 51, No. 1. pp. 132-137.
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abstract = "Background: Pre-β1-HDL participates in a cyclic process involved in the retrieval of cholesterol from peripheral tissues. Although pre-β1-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 °C in the presence of aprotinin (final concentration, 50 kIU/L). The lipid-poor apo A-I concentration decreased during incubation at 37 °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-β1-HDL measured by other methods.",
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Suzuki, M, Wada, H, Maeda, S, Saito, K, Minatoguchi, S, Saito, K & Seishima, M 2005, 'Increased plasma lipid-poor apolipoprotein A-I in patients with coronary artery disease', Clinical Chemistry, vol. 51, no. 1, pp. 132-137. https://doi.org/10.1373/clinchem.2004.041012

Increased plasma lipid-poor apolipoprotein A-I in patients with coronary artery disease. / Suzuki, Makiko; Wada, Hisayasu; Maeda, Satoshi; Saito, Kuniaki; Minatoguchi, Shinya; Saito, Kazunori; Seishima, Mitsuru.

In: Clinical Chemistry, Vol. 51, No. 1, 01.01.2005, p. 132-137.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Increased plasma lipid-poor apolipoprotein A-I in patients with coronary artery disease

AU - Suzuki, Makiko

AU - Wada, Hisayasu

AU - Maeda, Satoshi

AU - Saito, Kuniaki

AU - Minatoguchi, Shinya

AU - Saito, Kazunori

AU - Seishima, Mitsuru

PY - 2005/1/1

Y1 - 2005/1/1

N2 - Background: Pre-β1-HDL participates in a cyclic process involved in the retrieval of cholesterol from peripheral tissues. Although pre-β1-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 °C in the presence of aprotinin (final concentration, 50 kIU/L). The lipid-poor apo A-I concentration decreased during incubation at 37 °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-β1-HDL measured by other methods.

AB - Background: Pre-β1-HDL participates in a cyclic process involved in the retrieval of cholesterol from peripheral tissues. Although pre-β1-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 °C in the presence of aprotinin (final concentration, 50 kIU/L). The lipid-poor apo A-I concentration decreased during incubation at 37 °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-β1-HDL measured by other methods.

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