Altered particle size distribution of apolipoprotein A-I-containing lipoproteins in subjects with coronary artery disease

Cheung, MC; Brown, B. Greg; Wolf, AC; Jj, Albers

doi:10.1016/s0022-2275(20)42061-9

Cited by 188 publications

(9 citation statements)

References 40 publications

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“…It has been proposed that LpA-I may be more directly protective against the development of atherosclerosis than LpA-I:A-II (Fruchart & Ailhaud, 1992). Although this has been controversial (Cheung et al, 1991), recent epidemiologic data suggest that LpA-I is a better predictor of coronary heart disease risk than LpA-I:A-II (Parra et al, 1992). In addition, an apoA-I-containing subfraction with pre-/S mobility has been proposed as a primary acceptor for the cholesterol derived from cells (Castro & Fielding, 1988).…”

Section: Resultsmentioning

confidence: 99%

Biochemical characterization of the three major subclasses of lipoprotein A-I preparatively isolated from human plasma

Duverger¹,

Rader²,

Duchâteau³

et al. 1993

Biochemistry

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Apolipoprotein (apo) A-I is the major protein constituent of plasma high-density lipoproteins (HDL). HDL consist of two major classes of apoA-I-containing lipoproteins: LpA-I and LpA-I:A-II. LpA-I includes heterogeneous lipoprotein particles that differ in size and hydrated density. LpA-I was isolated by immunoaffinity chromatography from the fasting plasma of 24 normal human subjects and separated by gel filtration chromatography. Three major subclasses of LpA-I were eluted: large (Lg-LpA-I), medium (Md-LpA-I), and small LpA-I (Sm-LpA-I). By nondenaturing gradient PAGE, Lg-LpA-I, Md-LpA-I, and Sm-LpA-I had mean Strokes diameters of 10.8 +/- 0.5, 8.9 +/- 0.5, and 7.5 +/- 0.3 nm, respectively. The lipid/protein ratios were 1.25 +/- 0.12 for Lg-LpA-I, 0.75 +/- 0.10 for Md-LpA-I, and 0.38 +/- 0.08 for Sm-LpA-I. Lg-LpA-I was relatively lipid and cholesteryl ester rich compared with Md-LpA-I and Sm-LpA-I. Sm-LpA-I contained phospholipids as the major lipid component. ApoA-I was the major apolipoprotein in all LpA-I subfractions, whereas apoE was present only in Lg-LpA-I and apoA-IV was associated with both Md-LpA-I and Sm-LpA-I. All three LpA-I subclasses exhibited predominantly alpha mobility on agarose electrophoresis. Lg-LpA-I migrated as a diffuse band in the fast alpha position, whereas Md-LpA-I and Sm-LpA-I migrated to the slow alpha position.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Resultsmentioning

confidence: 99%

Biochemical characterization of the three major subclasses of lipoprotein A-I preparatively isolated from human plasma

Duverger¹,

Rader²,

Duchâteau³

et al. 1993

Biochemistry

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“…For the PAGE analysis, 20 l of plasma and 10 l of high-molecularweight standards (Pharmacia Biotech, Piscataway, NJ) were electrophoresed on preformed 4-30% polyacrylamide gels (Alamo Gels, San Antonio, TX) in 0.09 M Tris, 0.08 M boric acid, 0.003 M EDTA, pH 8.35, at 200 V for 20 h at 4°C. Lipoproteins and molecular weight standards were visualized with Sudan Black B and Coomassie G250, respectively, and scanned with a laser densitometer (LKB Ultroscan XL) as described previously (8). For the FPLC analysis, two Superose columns, Superose 6 and Superose 12 (Pharmacia Biotech), were connected in series and equilibrated in 10 mM Tris, 1 mM EDTA, 150 mM NaCl, pH 7.4.…”

Section: Methodsmentioning

confidence: 99%

Quantitative trait locus mapping of genes that regulate HDL cholesterol in SM/J and NZB/B1NJ inbred mice

Pitman

Korstanje

Churchill

et al. 2002

Physiological Genomics

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To investigate the quantitative trait loci (QTL) regulating plasma cholesterol, the female progeny of an (SMxNZB/ B1NJ)xNZB/B1NJ backcross were fed an atherogenic diet. After 18 wk, plasma total cholesterol and high-density lipoprotein cholesterol (HDL-C) was measured. HDL-C concentrations were greater in NZB than in SM mice. For standard chow-fed mice, QTL were found near D5Mit370 and D18Mit34. For mice fed an atherogenic diet, a QTL was found near D5Mit239. The QTL for chow-fed and atherogenic-fed mice on chromosome 5 seem to be two different loci. We used a multitrait analysis to rule out pleiotropy in favor of a two-QTL hypothesis. Furthermore, the HDL-C in these strains was induced by the high-fat diet. For inducible HDL-C, one significant locus was found near D15Mit39. The gene for an HDL receptor, Srb1, maps close to the HDL-C QTL at D5Mit370, but the concentrations of Srb1 mRNA and SR-B1 protein and the gene sequence of NZB/B1NJ and SM/J did not support Srb1 as a candidate gene. With these QTL, we have identified chromosomal regions that affect lipoprotein profiles in these strains.

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“…Non-denaturing polyacrylamide gradient gel electrophoresis was used to analyze the HDL particle size distribution. Electrophoresis was performed on 20 l of mouse plasma and 10 l of high molecular weight standards (Pharmacia Biotech, Inc., Piscataway, NJ), using 4-30% preformed polyacrylamide gel (Alamo Gels, Inc., San Antonio, TX) in 0.09 m Tris, 0.08 m boric acid, 0.003 m EDTA, pH 8.35, at 200 volts for 20 hours at 4 Њ C. Lipoproteins and the molecular weight standards were visualized with Sudan Black B and Coomassie G250, respectively, and scanned with a densitometer (LKB Ultrascan XL Laser Densitometer) as described (28).…”

Section: Non-denaturing Gradient Gel Electrophoresismentioning

confidence: 99%

Relationship between phospholipid transfer protein activity and HDL level and size among inbred mouse strains

Albers

Pitman

Wolfbauer

et al. 1999

Journal of Lipid Research

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Because of the paucity of data on phospholipid transfer protein (PLTP) activity and lipoprotein phospholipid in mouse strains, plasma PLTP activity (PLTA), plasma phospholipid and cholesterol, HDL phospholipid and cholesterol, and HDL size distribution were determined in 15 inbred mouse strains. The 15 inbred mouse strains differed in their relatedness to one another and consisted of six largely unrelated groups: Castaneus, Swiss, C57BL, AKR, DBA, and NZB. Lipid and PLTA analyses were performed on plasma pools from male and female mice that had fasted for 4 h prior to blood draw. Among the representative unrelated strains fed the chow diet, there was a highly significant relationship between PLTA and plasma phospholipid ( r s ‫؍‬ 0.727, P Ͻ 0.01), HDL phospholipid ( r s ϭ 0.762, P Ͻ 0.01), HDL cholesterol ( r s ‫؍‬ 0.699, P Ͻ 0.02), percentage of large HDL particles ( r s ϭ 0.699, P Ͻ 0.02), and HDL peak size ( r s ‫؍‬ 0.776, P Ͻ 0.01). Similar results were obtained among these strains fed a high fat, high cholesterol diet. PLTA increased in all strains fed the high fat diet ( ‫؍‬ 94%, range 6 to 221%). Strain SM having relatively low PLTA and HDL was crossed with strain NZB having high PLTA and HDL. The F1 progeny from this cross were backcrossed to strain SM and 41 male backcross progeny collected. Among these individual backcrossed animals, PLTA was highly correlated with plasma phospholipid ( r s ‫؍‬ 0.508, P ‫؍‬ 0.001), HDL phospholipid ( r s ‫؍‬ 0.566, P Ͻ 0.001), HDL cholesterol ( r s ‫؍‬ 0.532, P Ͻ 0.001), and percentage of large HDL particles ( r s ‫؍‬ 0.446, P ‫؍‬ 0.020). Therefore, we conclude that PLTP is a determinant of HDL level and size in mice.

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Altered particle size distribution of apolipoprotein A-I-containing lipoproteins in subjects with coronary artery disease

Cited by 188 publications

References 40 publications

Biochemical characterization of the three major subclasses of lipoprotein A-I preparatively isolated from human plasma

Biochemical characterization of the three major subclasses of lipoprotein A-I preparatively isolated from human plasma

Quantitative trait locus mapping of genes that regulate HDL cholesterol in SM/J and NZB/B1NJ inbred mice

Relationship between phospholipid transfer protein activity and HDL level and size among inbred mouse strains

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