Enzyme-linked immunosorbent assay of lipoprotein(a) in serum and cord blood

Abe, Akira; Maeda, Shin; Makino, Kazuhiko; Seishima, Mitsuru; Shimokawa, Kuniyasu; Noma, Akio; Kawade, Masato

doi:10.1016/0009-8981(88)90304-x

Cited by 58 publications

(16 citation statements)

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“…No difference of their levels was found in each of the 13 year groups in the children ( Figure 2) [41]. The fact that ox-Lp(a) and Lp(a)-IC were present in all the healthy children and especially in newborns was also supported by other studies [42][43][44], and anti-ox-LDL antibodies and LDL-IC were also easily detectable in asymptomatic young adults and children [45,46], suggesting that the immune response to modified lipoproteins could appear very early in the process, perhaps play an initiating role in atherosclerotic process.…”

Section: The Clinical Value Of Circulating Oxidized Lp(a)supporting

confidence: 73%

Lipoprotein(a) Oxidation, Autoimmune and Atherosclerosis

Wang¹

2012

Coronary Artery Disease - New Insights and Novel Approaches

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IntroductionLipoprotein(a) [Lp(a)] is a plasma lipoprotein whose structure and composition closely resembles that of low density lipoprotein (LDL), but with one of additional molecule of apolipoprotein(a) [apo(a)], a large glycoprotein linked to apoB by a disulfide bond (Figure 1) [1,2]. High Lp(a) levels have been established as an independent risk factor for atherocslerosis [3][4][5], and Lp(a) deposits have been found in atherosclerotic lesions but not in normal arterial walls [6][7][8].Lp(a) can be modified by oxidation in vitro, and then be taken up by macrophages by means of scavenger receptors, where it promotes their transformation into foam cells within the arterial walls [9][10][11][12][13]. Oxidized Lp(a) [ox-Lp(a)] may also induce adhesion molecular expression on monocytes, promoting their recruitment and adhesion to the endothelium [14], and influence the responsiveness of platelets to various agonists [15]. Modified forms of Lp(a), some resembling oxidized Lp(a), have been identified in human atheromatous lesions [16]. In addition, ox-Lp(a) causes significant changes in apo(a) conformation, which could enhance the interaction of these particles with plasminogen binding sites as well as macrophage scavenger receptors, resulting in increased inhibitory effect on plasminogen activation and finally leading to attenuate fibrinolytic activity [17].Ox-Lp(a) has been reported to play more potent role than native Lp(a) in atherosclerosis [10,14,17,18], and autoantibodies against ox-Lp(a), Lp(a) immune complexes [Lp(a)-IC] have also been detected in vivo simultaneously [19,20]. The present review article focuses specifically on the relationship between Lp(a) oxidation, autoimmune and atherosclerosis together with our recent work. The pathogenic role of oxidized Lp(a)Lp(a) contains a large specific glycoprotein called apo(a), attached by a single disulfide bridge to apoB 100 of LDL (Figure 1). The adverse cardiovascular qualities of Lp(a) have been related to both its LDL-like properties (i.e., formation of foam cells) and its presumed role in fibrinolysis. www.intechopen.comCoronary Artery Disease -New Insights and Novel Approaches 50 Lp(a) oxidationThe structure, fatty acid composition, and antioxidant concentrations of Lp(a) and LDL are quite similar [21]. In vitro studies have shown that Lp(a) can be modified by oxidation (both chemical and cellular-mediated) in a fashion similar to LDL [22]. This modification, which involved lipid peroxidation measured as thiobarbituric acid-reactive substances (TBARS), caused marked changes in the structure and biological properties of Lp(a). Relative to native Lp(a), oxidized particles showed decreases of free amino groups and protein fragmentation, increased negative charge, and high aggregation ability. They were taken up and degraded readily by human monocyte/macrophages by means of scavenger receptors, a known pathway for clearance of ox-LDL in atheroma, inducing cholesteryl ester accumulation and promoting their transformation into foam cells within the arterial w...

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Section: The Clinical Value Of Circulating Oxidized Lp(a)supporting

confidence: 73%

Lipoprotein(a) Oxidation, Autoimmune and Atherosclerosis

Wang¹

2012

Coronary Artery Disease - New Insights and Novel Approaches

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“…14 - 15 Detection limit was 0.5 mg/dL for Lp(a), and Lp(a) was quantified between 1 and 100 mg/dL. The reproducibility and accuracy of the assay were repeatedly verified; intra-assay and interassay coefficients of variation were 2.33-4.88% and 2.94-5.14%, respectively.…”

Section: Methodsmentioning

confidence: 89%

Lipoprotein(a) and ischemic cerebrovascular disease in young adults.

Nagayama

Shinohara

Nagayama

1994

Stroke

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Background and Purpose Serum lipoprotein(a) level is genetically determined and remains almost constant throughout life. Based on this property, we investigated the serum lipoprotein(a) levels of ischemic stroke patients in the chronic stage (mean period after stroke, 27 months) and its relation to the types of ischemic stroke.Methods We measured serum lipoprotein(a) levels in 101 patients with chronic ischemic stroke and 37 normal control subjects, taking the clinical profiles into consideration.Results Lipoprotein(a) levels in patients with atherothrombotic stroke were 28.0±19.6 mg/dL (mean±SD), which were significantly (/ > <.01) higher than those in patients with lacunar stroke and in normal control subjects (16.4±13.5 and 11.7±10.5 mg/dL, respectively). The lipoprotein(a) levels in patients with atherothrombotic stroke were significantly higher

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“…27 Serum Lp(a) was determined by enzymelinleed immunosorbent assay (ELISA) using a Tint Eliza Lp(a) kit (Biopool, Sweden). 28 For all measurements in our laboratory, the interassay and intra-assay coefficients of variation were less than 7% and 5%, respectively, and blinded quality-control specimens were included in each assay.…”

Section: Coronary Angiographymentioning

confidence: 99%

Associations Among Serum Lipoprotein(a) Levels, Apolipoprotein(a) Phenotypes, and Myocardial Infarction in Patients With Extremely Low and High Levels of Serum Lipoprotein(a)

Saku

Zhang

et al. 1999

Jpn Circ J

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ipoprotein(a) [Lp(a)] is a heterogeneous lipoprotein 1 that incorporates a low-density lipoprotein (LDL) particle and highly polymorphic apolipoprotein (a) [apo(a)], which is covalently linked to the apolipoprotein B moiety of the LDL by a single disulfide bridge. 2,3 Apo(a) is highly homologous to plasminogen and affects the human coagulation system. 4,5 The apo(a) gene locus is the major gene that controls plasma Lp(a) concentrations. 6,7 The alleles at this locus determine the size polymorphism of apo(a), which is the result of a variable number of expressed Japanese Circulation Journal Vol.63, September 1999 kringle IV repeats, 6-8 and is assessed by apo(a) genotyping. 7 Utermann et al first reported a size polymorphism of 6 apo(a) isoforms with different molecular weights, 8 and other researchers have detected additional apo(a) isoforms using different detection methods. 9,10 We recently detected 26 different apo(a) alleles, including a null allele, at the apo(a) locus by a sensitive high-resolution technique using sodium dodecyl sulfate (SDS)-agrose/gradient polyacrylamide gel electrophoresis (PAGE). 11 Approximately 75% of the subjects had a double band of apo(a), and the remaining subjects had a single band. An inverse relationship has been demonstrated between plasma Lp(a) concentrations and the size of apo(a), 8,11 and a smaller Lp(a) band was well correlated with Lp(a) levels in double-banded phenotypes. [11][12][13] High plasma levels of Lp(a) have been shown to be associated with myocardial infarction (MI), 14-17 although this association was not confirmed by 2 prospective studies. 18,19 Apo(a) size polymorphism has been shown to be inversely associated with the risk of coronary heart disease (CHD) in Jpn Circ J 1999; 63: 659 -665 (Received April 2, 1999; revised manuscript received May 24, 1999; accepted May 27, 1999 , age: 62±10 y) and control subjects (n=92, M/F: 53/39, age: 58±14 y) were classified into quintile groups (Groups I to V) according to Lp(a) levels. Apo(a) isoform phenotyping was performed by a sensitive, high-resolution technique using sodium dodecyl sulfate-agarose/gradient polyacrylamide gel electrophoresis (3-6%), which identified 26 different apo(a) phenotypes, including a null type. Groups with higher Lp(a) levels (Groups II, III, and V) had higher percentages of MI patients than that with the lowest Lp(a) levels (Group I) (54%, 56%, or 75% vs. 32%, p<0.05). Groups with different Lp(a) levels had different frequency distributions of apo(a) isoprotein phenotypes: Groups II, III, IV, and V, which had increasing Lp(a) levels, had increasingly higher percentages of smaller isoforms (A1-A4, A5-A9) and decreasingly lower percentages of large isoforms (A10-A20, A21-A25) compared to Group I. An apparent inverse relationship existed between Lp(a) and the apo(a) phenotype. Subjects with the highest Lp(a) levels (Group V) had significantly (p<0.05) higher serum levels of total cholesterol, apo B, and Lp(a). Patients with MI and the controls had different distributions of apo(a) phenot...

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Enzyme-linked immunosorbent assay of lipoprotein(a) in serum and cord blood

Cited by 58 publications

References 13 publications

Lipoprotein(a) Oxidation, Autoimmune and Atherosclerosis

Lipoprotein(a) Oxidation, Autoimmune and Atherosclerosis

Lipoprotein(a) and ischemic cerebrovascular disease in young adults.

Associations Among Serum Lipoprotein(a) Levels, Apolipoprotein(a) Phenotypes, and Myocardial Infarction in Patients With Extremely Low and High Levels of Serum Lipoprotein(a)

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