Plasminogen activator inhibitor-1 polymorphisms (?44 G>A and HindIII C>G) in systemic lupus erythematosus: association with clinical variables
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  • 作者:Jorge Ramón Padilla-Gutiérrez (1) (2)
    Claudia Azucena Palafox-Sánchez (1)
    Yeminia Valle (1) (2)
    Gerardo Orozco-Barocio (3)
    Edith Oregón-Romero (1)
    Mónica Vázquez-Del Mercado (1)
    Héctor Rangel-Villalobos (4)
    Mara Anaís Llamas-Covarrubias (1)
    José Francisco Mu?oz-Valle (1)
  • 关键词:PAI ; 1 ; Polymorphisms ; Haplotypes ; SLE
  • 刊名:Clinical and Experimental Medicine
  • 出版年:2011
  • 出版时间:March 2011
  • 年:2011
  • 卷:11
  • 期:1
  • 页码:11-17
  • 全文大小:224KB
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  • 作者单位:Jorge Ramón Padilla-Gutiérrez (1) (2)
    Claudia Azucena Palafox-Sánchez (1)
    Yeminia Valle (1) (2)
    Gerardo Orozco-Barocio (3)
    Edith Oregón-Romero (1)
    Mónica Vázquez-Del Mercado (1)
    Héctor Rangel-Villalobos (4)
    Mara Anaís Llamas-Covarrubias (1)
    José Francisco Mu?oz-Valle (1)

    1. Instituto de Investigación en Reumatología y del Sistema Músculo Esquelético, Departamento de Biología Molecular y Genómica, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Insurgentes 244-1, Colonia Lomas de Atemajac, 45178, Zapopan, Jalisco, México
    2. Posdoctoral Fellow in Biomedical Sciences (Immunology). Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Guadalajara, Jalisco, México
    3. Departamento de Inmunología y Reumatología del Hospital General de Occidente, Secretaría de Salud Jalisco, Av. Zoquipan 1050, 45100, Zapopan, Jalisco, México
    4. Instituto de Investigación en Genética Molecular, Centro Universitario de la Ciénega, Universidad de Guadalajara, Ocotlán, Jalisco, México
文摘
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by the presence of autoantibodies against nuclear autoantigens as well as cytoplasmic and circulating proteins. Recent studies have demonstrated mechanisms responsible for modulation of the immune response by the plasminogen activator inhibitor-1 (PAI-1). Furthermore, the endogenous PAI-1 has shown to promote a Th2 immune response. We assessed the ?44 G>A and HindIII C>G PAI-1 polymorphisms in SLE. In a case–control study of 71 SLE patients classified according to ACR criteria and 71 healthy subjects (HS). The A allele of ?44 PAI-1 polymorphism showed a significant difference in SLE patients (41%) when compared with HS (27%) [P?=?0.01; OR?=?1.8, 95%, CI?=?1.1-.0]. In addition, the ?44 G>A PAI-1 polymorphism was associated with increased risk for SLE in a dominant genetic model (G/G vs. G/A?+?A/A; OR?=?2.3, 95% CI?=?1.14-.44). Also, anti-RNP positive antibodies in SLE were associated with G/G ?44 PAI-1 genotype. The HindIII polymorphism did not show any differences. The haplotype analysis showed that the AC haplotype confers susceptibility to SLE (OR?=?3.1, 95% CI, 1.45-.52; P?=?0.003). The AC haplotype of the ?44 and HindIII PAI-1 polymorphism might be an additional susceptibility factor to SLE in Mexicans.

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