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Proteomics and genetics aspects of aspirin resistance
被引:0
作者:
Mateos-Caceres, P. J.
[1
]
Azcona, L.
[1
]
Fernandez-Ortiz, A.
[2
]
Sacristan, D.
[1
]
Bernardo, E.
[2
]
Ramos-Mozo, P.
[1
]
Alonso-Orgaz, S.
[1
]
Fernandez-Arquero, M.
[3
]
Lopez-Farre, A.
[1
]
Macaya, C.
[1
,2
]
机构:
[1] Hosp Clin San Carlos, Unidad Invest Cardiovasc, Profesor Martin Lagos S-N, Madrid 28040, Spain
[2] Hosp Clin San Carlos, Unidad Coronaria, Madrid, Spain
[3] Hosp Clin San Carlos, Inst Cardiovasc, Dept Inmunol, Madrid, Spain
来源:
TRAUMA-SPAIN
|
2008年
/
19卷
/
03期
关键词:
Aspirin resistance;
proteomics;
genetic polymorphisms;
D O I:
暂无
中图分类号:
R4 [临床医学];
学科分类号:
1002 ;
100602 ;
摘要:
Aim: To evaluate the existence of a possible association between Aspirin resistance (AR), COX-1 single-nucleotide polymorphisms (SNPs) and the modifications in the plasma proteome of clinically stable coronary patients. Materials and methods: AR was defined according to the PFA-100 assay. AR-sensitive and AR-resistant patients had been taken aspirin for the last 9 months. The proteomic study (19 AR-sensitive, 19 AR-resistant) was performed using IPG strips (17cm, pH 4-7), SDS-PAGE gels (10%) and silver staining. We study three SNPs (A842G, C22T y C50T) in 50 AR-sensitive patients, 33 AR-resistant and 83 controls using a real-time PCR. Results: The expression of four .1-antitripsin isoforms was increased in the aspirin-resistant patients. No differences were found in the expression of ceruloplasmin, haptoglobin-precursor, apolipoprotein-AI and albumin-precursor between both groups of patients. The A-842G SNP was undetectable in all subjects. The remaining two SNPs (C22T y C50T) showed a low frequency with respect the global population. Conclusions: The low SNPs frequencies were unlikely to explain the difference in aspirin responsiveness between both groups of patients. The changes in .1-antitripsin could be linked with a different inflammatory state in these patients.
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页码:143 / 151
页数:9
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