A prospective evaluation of apolipoprotein M gene T-778C polymorphism in relation to coronary artery disease in Han Chinese

Jiao, Guoqing; Zhang, Yuan; Xue, Yong-sheng; Yang, Chengjian; Chengbao, LU; Lüˇ, Zhi-qian; Xiao, Mengli

doi:10.1016/j.clinbiochem.2007.04.023

Cited by 34 publications

(28 citation statements)

References 16 publications

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“…A subsequent case-control study showed that CHD patients had an increased frequency of the SNP T-778C allele compared with controls (18). The T-855C allele was also recently linked to CHD when carriers of the C allele were found to have an increased risk of CHD compared with the wild-type TT genotype (19).…”

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Levels of apolipoprotein M are not associated with the risk of coronary heart disease in two independent case-control studies

Ahnström

Axler

Jauhiainen

et al. 2008

Journal of Lipid Research

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Apolipoprotein M (apoM), a 25 kDa plasma protein belonging to the lipocalin protein family, is predominantly associated with HDL. Studies in mice have suggested apoM to be important for the formation of pre-b-HDL and to increase cholesterol efflux from macrophage foam cells. Overexpression of human apoM in LDL receptor-deficient mice reduced the atherogenic effect of a cholesterol-rich diet. The aim of the present study was to investigate whether the apoM levels in man predict the risk for coronary heart disease (CHD). ApoM was measured in samples from two separate case-control studies. FINRISK ʼ92 consisted of 255 individuals, of whom 80 developed CHD during followup and 175 were controls. The Copenhagen City Heart Study included 1,865 individuals, of whom 921 developed CHD during follow-up and 944 were controls. Correlation studies of apoM concentration with several analytes showed a marked positive correlation with HDL and total cholesterol as well as with apoA-I and apoB. There was no significant difference in mean apoM level between CHD and control subjects in either study. In conditional logistic regression analyses, apoM was not a predictor of CHD events, [odds ratio (95% CI) 0.97 (0.74-1.27) and 0.92 (0.84-1.02), respectively]. In conclusion, no association between apoM and CHD could be found in this study.-Ahnström, J., O. Axler, M. Jauhiainen, V. Salomaa, A. S. Havulinna, C. Ehnholm, R. Frikke-Schmidt, A. Tybjaerg-Hansen, and B. Dahlbäck. Levels of apolipoprotein M are not associated with the risk of coronary heart disease in two independent case-control studies.

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confidence: 99%

Levels of apolipoprotein M are not associated with the risk of coronary heart disease in two independent case-control studies

Ahnström

Axler

Jauhiainen

et al. 2008

Journal of Lipid Research

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“…Genetic association studies in Chinese populations have associated two single-nucleotide polymorphisms located in the apoM proximal promoter region (single-nucleotide polymorphisms T-778C and SNP T-855C) with the development of coronary artery disease (26,27). The T-778C polymorphism was also found to be associated with types 1 and 2 diabetes in Chinese populations supporting the possible involvement of apoM in the pathogenesis of diabetes as suggested by the reduced apoM expression levels found in animal models of diabetes and some patients with diabetes and metabolic syndrome (22, 28 -34).…”

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Regulation of Human Apolipoprotein M Gene Expression by Orphan and Ligand-dependent Nuclear Receptors

Mosialou

Zannis

Kardassis

2010

Journal of Biological Chemistry

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Apolipoprotein M (apoM) plays an important role in the biogenesis and the metabolism of anti-atherogenic HDL particles in plasma and is expressed primarily in the liver and the kidney. We investigated the role of hormone nuclear receptors in apoM gene regulation in hepatic cells. Overexpression via adenovirusmediated gene transfer and siRNA-mediated gene silencing established that hepatocyte nuclear factor 4 (HNF-4) is an important regulator of apoM gene transcription in hepatic cells. apoM promoter deletion analysis combined with DNA affinity precipitation and chromatin immunoprecipitation assays revealed that HNF-4 binds to a hormone-response element (HRE) in the proximal apoM promoter (nucleotides ؊33 to ؊21). Mutagenesis of this HRE decreased basal hepatic apoM promoter activity to 10% of control and abolished the HNF4-mediated transactivation of the apoM promoter. In addition to HNF-4, homodimers of retinoid X receptor and heterodimers of retinoid X receptor with receptors for retinoic acid, thyroid hormone, fibrates (peroxisome proliferator-activated receptor), and oxysterols (liver X receptor) were shown to bind with different affinities to the proximal HRE in vitro and in vivo. Ligands of these receptors strongly induced human apoM gene transcription and apoM promoter activity in HepG2 cells, whereas mutations in the proximal HRE abolished this induction. These findings provide novel insights into the role of apoM in the regulation of HDL by steroid hormones and into the development of novel HDL-based therapies for diseases such as diabetes, obesity, metabolic syndrome, and coronary artery disease that affect a large proportion of the population in Western countries.

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“…A SNP (rs805296) located in APOM promoter region near rs805297 was also found to be significantly associated with RA. SNP rs805296 has been implicated in some diseases such as coronary artery disease and type 1 diabetes mellitus (T1DM), but not in RA (Jiao et al, 2007;Wu et al, 2009). Given that T1DM is an autoimmune disease and that there is a higher risk of atherosclerosis in RA patients than normal individuals, we could assume that APOM promoter polymorphism SNP rs805296 may also be involved in both autoimmune mediated-and inflammation mediated-diseases.…”

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Common variants at the promoter region of theAPOMconfer a risk of rheumatoid arthritis

Jin

Yim

et al. 2011

Exp Mol Med

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Although the genetic component in the etiology of rheumatoid arthritis (RA) has been consistently suggested, many novel genetic loci remain to uncover. To identify RA risk loci, we performed a genome-wide association study (GWAS) with 100 RA cases and 600 controls using Affymetrix SNP array 5.0. The candidate risk locus (APOM gene) was re-sequenced to discover novel promoter and coding variants in a group of the subjects. Replication was performed with the independent case-control set comprising of 578 RAs and 711 controls. Through GWAS, we identified a novel SNP associated with RA at the APOM gene in the MHC class III region on 6p21.33 (rs805297, odds ratio (OR) = 2.28, P = 5.20 × 10 -7). Three more polymorphisms were identified at the promoter region of the APOM by the re-sequencing. For the replication, we genotyped the four SNP loci in the independent case-control set. The association of rs805297 identified by GWAS was successfully replicated (OR = 1.40, P = 6.65 × 10 -5). The association became more significant in the combined analysis of discovery and replication sets (OR = 1.56, P = 2.73 × 10 -10). The individuals with the rs805297 risk allele (A) at the promoter region showed a significantly lower level of APOM expression compared with those with the protective allele (C) homozygote. In the logistic regressions by the phenotype status, the homozygote risk genotype (A/A) consistently showed higher ORs than the heterozygote one (A/C) for the phenotype-positive RAs. These results indicate that APOM promoter polymorphisms are significantly associated with the susceptibility to RA.

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A prospective evaluation of apolipoprotein M gene T-778C polymorphism in relation to coronary artery disease in Han Chinese

Cited by 34 publications

References 16 publications

Levels of apolipoprotein M are not associated with the risk of coronary heart disease in two independent case-control studies

Levels of apolipoprotein M are not associated with the risk of coronary heart disease in two independent case-control studies

Regulation of Human Apolipoprotein M Gene Expression by Orphan and Ligand-dependent Nuclear Receptors

Common variants at the promoter region of theAPOMconfer a risk of rheumatoid arthritis

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