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| [PMID]: | 28449647 |
| [Au] Autor: | Yang WY; Petit T; Cauwenberghs N; Zhang ZY; Sheng CS; Thijs L; Salvi E; Izzi B; Vandenbriele C; Wei FF; Gu YM; Jacobs L; Citterio L; Delli Carpini S; Barlassina C; Cusi D; Hoylaerts MF; Verhamme P; Kuznetsova T; Staessen JA |
| [Ad] Endereço: | Studies Coordinating Centre, Research Unit Hypertension and Cardiovascular Epidemiology, KU Leuven Department of Cardiovascular Sciences,, University of Leuven, Campus Sint Rafaël, Kapucijnenvoer 35, Box 7001, BE-3000, Leuven, Belgium. |
| [Ti] Título: | PEAR1 is not a major susceptibility gene for cardiovascular disease in a Flemish population. |
| [So] Source: | BMC Med Genet;18(1):45, 2017 04 27. | | [Is] ISSN: | 1471-2350 |
| [Cp] País de publicação: | England |
| [La] Idioma: | eng |
| [Ab] Resumo: | BACKGROUND: Platelet Endothelial Aggregation Receptor 1 (PEAR1), a membrane protein highly expressed in platelets and endothelial cells, plays a role in platelet contact-induced activation, sustained platelet aggregation and endothelial function. Previous reports implicate PEAR1 rs12041331 as a variant influencing risk in patients with coronary heart disease. We investigated whether genetic variation in PEAR1 predicts cardiovascular outcome in a white population. METHODS: In 1938 participants enrolled in the Flemish Study on Environment, Genes and Health Outcomes (51.3% women; mean age 43.6 years), we genotyped 9 tagging SNPs in PEAR1, measured baseline cardiovascular risk factors, and recorded Cardiovascular disease incidence. For SNPs, we contrasted cardiovascular disease incidence of minor-allele heterozygotes and homozygotes (variant) vs. major-allele homozygotes (reference) and for haplotypes carriers vs. non-carriers. In adjusted analyses, we accounted for family clusters and baseline covariables, including sex, age, body mass index, mean arterial pressure, the total-to-HDL cholesterol ratio, smoking and drinking, antihypertensive drug treatment, and history of cardiovascular disease and diabetes mellitus. RESULTS: Over a median follow-up of 15.3 years, 238 died and 181 experienced a major cardiovascular endpoint. The multivariable-adjusted hazard ratios of eight PEAR1 SNPs, including rs12566888, ranged from 0.87 to 1.07 (P ≥0.35) and from 0.78 to 1.30 (P ≥0.15), respectively. The hazard ratios of three haplotypes with frequency ≥10% ranged from 0.93 to 1.11 (P ≥0.49) for mortality and from 0.84 to 1.03 (P ≥0.29) for a cardiovascular complications. These results were not influenced by intake of antiplatelet drugs, nonsteroidal anti-inflammatory drugs, or both (P-values for interaction ≥ 0.056). CONCLUSIONS: In a White population, we could not replicate previous reports from experimental studies or obtained in patients suggesting that PEAR1 might be a susceptibility gene for cardiovascular complications. |
| [Mh] Termos MeSH primário: |
Doenças Cardiovasculares/genética
Predisposição Genética para Doença
Receptores de Superfície Celular/genética
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| [Mh] Termos MeSH secundário: |
Adulto
Bélgica
Feminino
Haplótipos
Seres Humanos
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
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| [Pt] Tipo de publicação: | JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T |
[Nm] Nome de substância:
| 0 (PEAR1 protein, human); 0 (Receptors, Cell Surface) |
| [Em] Mês de entrada: | 1706 |
| [Cu] Atualização por classe: | 171231 |
[Lr] Data última revisão:
| 171231 |
| [Sb] Subgrupo de revista: | IM |
| [Da] Data de entrada para processamento: | 170429 |
| [St] Status: | MEDLINE |
| [do] DOI: | 10.1186/s12881-017-0411-x |
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