Plasminogen activator inhibitor-1 C/G polymorphism in relation to plasma levels in rheumatoid arthritis

被引:6
|
作者
Torres-Carrillo, Norma [1 ]
Torres-Carrillo, Nora Magdalena [1 ]
Martinez-Bonilla, Gloria Esther [2 ]
Vazquez-Del Mercado, Monica [1 ]
Palafox-Sanchez, Claudia Azucena [1 ]
Oregon-Romero, Edith [1 ]
Bernard-Medina, Ana Guilaisne [2 ]
Rangel-Villalobos, Hector [3 ]
Munoz-Valle, Jose Francisco [1 ]
机构
[1] Univ Guadalajara, Dept Biol Mol & Genom, Inst Invest Reumatol & Sistema Musculo Esquelet, Ctr Univ Ciencias Salud, Guadalajara 44430, Jalisco, Mexico
[2] OPD Hosp Civil Guadalajara Fray Antonio Alcalde, Serv Reumatol, Guadalajara, Jalisco, Mexico
[3] Univ Guadalajara, Inst Genet Mol, Ctr Univ Cienega, Ocotlan, Jalisco, Mexico
关键词
PAI-1; Plasma levels; Polymorphism; Rheumatoid arthritis; CORONARY-ARTERY-DISEASE; GENE POLYMORPHISMS; PAI-1; MECHANISMS; INFLAMMATION; ASSOCIATION;
D O I
10.1007/s10238-009-0038-0
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Plasminogen activator inhibitor type 1 (PAI-1) is an inhibitor of plasmin production. Plasmin can directly or indirectly to degrade cartilage and bone matrix. The PAI-1 HindIII polymorphism has been associated with high PAI-1 plasma levels in myocardial infarction patients and control populations. Furthermore, it has been associated with the angiographic extent of coronary artery disease, but their involvement in other diseases is still uncertain. Here, we assessed the relationship between PAI-1 HindIII polymorphism and PAI-1 plasma levels in rheumatoid arthritis (RA). One hundred and twenty-five RA patients and 132 control subjects (CS) were included. Genotypes were identified by the polymerase chain reaction-restriction fragment length polymorphism technique and PAI-1 plasma levels were quantified using an ELISA kit. Not significant differences in genotype and allele frequencies between both studied groups were observed (P > 0.05). RA patients showed lower PAI-1 plasma levels (18.92 +/- A 12.94 ng/ml) than CS (23.68 +/- A 23.38 ng/ml), without significant difference (P = 0.299). However, in RA patients the C/G genotype carriers showed higher PAI-1 plasma levels (23.00 +/- A 13.81 ng/ml) with respect to C/C (16.77 +/- A 11.97 ng/ml) and G/G (10.47 +/- A 7.07 ng/ml) genotype carriers (P = 0.036). The PAI-1 HindIII polymorphism was not associated with RA susceptibility. However, the C/G genotype is associated with high PAI-1 plasma levels in RA patients.
引用
收藏
页码:223 / 228
页数:6
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