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.
引用
收藏
页码:143 / 151
页数:9
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