5' control regions of the apolipoprotein(a) gene and members of the related plasminogen gene family.

Wade, David P.; Clarke, John; Lindahl, Gisela; Liu, Alexander C.; Zysow, Bernice R.; Meer, Kelli; Schwartz, K.; Lawn, Richard M.

doi:10.1073/pnas.90.4.1369

Cited by 154 publications

(120 citation statements)

References 34 publications

(31 reference statements)

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“…It is assumed that large apo(a) isoforms are transcribed and translated much more slowly than small ones and that the secretion of large apo(a) is much less efficient than that of small apo(a), these events reflecting the plasma Lp(a) concentration. Finally it is apparent from recent studies that additional genetic factors related to the promoter region in apo(a) which are not discussed here have an impact on plasma Lp(a) concentrations [23,24]. In addition evidence is accumulating that rate of Lp(a) assembly is related to plasma Lp(a) levels, which is the main topic of this review.…”

Section: Metabolism Of Lp(a)mentioning

confidence: 90%

The assembly of lipoprotein Lp(a)

Frank¹,

Durovic²,

Kostner³

1996

Eur J Clin Investigation

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Section: Metabolism Of Lp(a)mentioning

confidence: 90%

The assembly of lipoprotein Lp(a)

Frank¹,

Durovic²,

Kostner³

1996

Eur J Clin Investigation

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“…Perhaps apo(a) was released from a preformed hepatic pool. For example, it is possible that release of OxPL from the plaque upregulates liver apo(a) synthesis, as the apo(a) gene has an IL-6 response element leading to enhanced transcription, 23 similar to the effect of cytokines that upregulate C-reactive protein synthesis. Patients with the highest baseline Lp(a) levels had the greatest absolute increases in Lp(a) after PCI.…”

Section: Tsimikas Et Al Oxldl and Lp(a) In Pci 3167mentioning

confidence: 99%

Percutaneous Coronary Intervention Results in Acute Increases in Oxidized Phospholipids and Lipoprotein(a)

et al. 2004

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Background-This study was performed to assess whether oxidized low-density lipoprotein (OxLDL) levels are elevated after percutaneous coronary intervention (PCI). Methods and Results-Patients (nϭ141) with stable angina pectoris undergoing PCI had serial venous blood samples drawn before PCI, after PCI, and at 6 and 24 hours, 3 days, 1 week, and 1, 3, and 6 months. Plasma levels of OxLDL-E06, a measure of oxidized phospholipid (OxPL) content on apolipoprotein B-100 detected by antibody E06, lipoprotein(a) [Lp(a)], autoantibodies to malondialdehyde (MDA)-LDL and copper-oxidized LDL (Cu-OxLDL), and apolipoprotein B-100 -immune complexes (apoB-IC) were measured. OxLDL-E06 and Lp(a) levels significantly increased immediately after PCI by 36% (PϽ0.0001) and 64% (PϽ0.0001), respectively, and returned to baseline by 6 hours. In vitro immunoprecipitation of Lp(a) from selected plasma samples showed that almost all of the OxPL detected by E06 was bound to Lp(a) at all time points, except in the post-PCI sample, suggesting independent release and subsequent reassociation of OxPL with Lp(a) by 6 hours. Strong correlations were noted between OxLDL-E06 and Lp(a) (rϭ0.68, PϽ0.0001). MDA-LDL and Cu-OxLDL autoantibodies decreased, whereas apoB-IC levels increased after PCI, but both returned to baseline by 6 hours. Subsequently, IgM autoantibodies increased and peaked at 1 month and then returned to baseline, whereas IgG autoantibodies increased steadily over 6 months. Conclusions-PCI results in acute plasma increases of Lp(a) and OxPL and results in short-term and long-term immunologic responses to OxLDL. OxPL that are released or generated during PCI are transferred to Lp(a), suggesting that Lp(a) may contribute acutely to a protective innate immune response. In settings of enhanced oxidative stress and chronically elevated Lp(a) levels, the atherogenicity of Lp(a) may stem from its capacity as a carrier of proinflammatory oxidation byproducts.

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“…31 A second example is the (tttta) n repeat polymorphism in the 5Ј flanking region of the lipoprotein(a) [Lp(a)] gene, which has been shown to be functional, 32 with constructs containing 8 copies of the repeat showing a 5-fold increase of transcriptional activity in vitro compared with constructs with 9 copies of the repeat. 33 …”

Section: Tetranucleotide Repeat and Cetp Expressionmentioning

confidence: 99%

Linkage of the Cholesteryl Ester Transfer Protein ( CETP ) Gene to LDL Particle Size

et al. 2000

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Background-A preponderance of small, dense LDL particles, elevated levels of plasma triglycerides (TG), and low levels of HDL characterize the atherogenic lipoprotein phenotype, which is associated with increased coronary artery disease (CAD) risk. Genetic and environmental factors influence LDL size, cholesteryl ester transfer protein (CETP) being one of the candidate genes. CETP mediates the transfer of cholesteryl ester from HDL to apolipoprotein (apo) B-containing lipoproteins in exchange for TG, promoting reverse cholesterol transfer and remodeling of lipoprotein particles. Methods and Results-We have identified a tetranucleotide repeat (fragment sizes from 324 to 464 bp; heterozygosity indexϭ0.74) within the CETP promoter and used it in quantitative sib-pair linkage analysis in 119 female dizygotic (DZ) twins. Linkage was found to LDL size (PϽ0.001), TG (PϽ0.005), and plasma apoB (Pϭ0.02). The distribution of the tetranucleotide repeats was bimodal, and there was strong allelic association of the "short" alleles with the B2 allele of CETP TaqIB polymorphic site (PϽ0.001). Conclusions-This report of linkage of the CETP gene to LDL particle size adds to the list of candidate genes linked to LDL size, supporting the hypothesis of multigenic determination of LDL size heterogeneity. Whether this promoter variation is itself functional or is a marker for a functional site in the CETP gene remains to be determined. (Circulation.

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5' control regions of the apolipoprotein(a) gene and members of the related plasminogen gene family.

Cited by 154 publications

References 34 publications

The assembly of lipoprotein Lp(a)

The assembly of lipoprotein Lp(a)

Percutaneous Coronary Intervention Results in Acute Increases in Oxidized Phospholipids and Lipoprotein(a)

Linkage of the Cholesteryl Ester Transfer Protein ( CETP ) Gene to LDL Particle Size

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