Association of the Smad3 and NFATc2 gene polymorphisms and their serum levels with susceptibility to rheumatoid arthritis in Polish cohorts

被引:13
|
作者
Paradowska-Gorycka, A. [1 ]
Romanowska-Prochnicka, K. [2 ]
Haladyj, E. [2 ]
Manczak, M. [3 ]
Maslinski, S. [4 ]
Olesinska, M. [2 ]
机构
[1] Inst Rheumatol, Dept Biochem & Mol Biol, PL-02637 Warsaw, Poland
[2] Inst Rheumatol, Dept Connect Tissue Dis, PL-02637 Warsaw, Poland
[3] Inst Rheumatol, Dept Epidemiol & Hlth Promot, PL-02637 Warsaw, Poland
[4] Med Univ Warsaw, Dept Pathophysiol, Warsaw, Poland
来源
CLINICAL AND EXPERIMENTAL IMMUNOLOGY | 2015年 / 179卷 / 03期
关键词
NFATc2; polymorphisms; rheumatoid arthritis; serum levels; Smad3; SYSTEMIC-LUPUS-ERYTHEMATOSUS; T-CELLS; TRANSCRIPTIONAL REGULATION; CLINICAL-FEATURES; NUCLEAR FACTOR; EXPRESSION; DISEASES; OSTEOARTHRITIS; NEPHROPATHY; PREDICTION;
D O I
10.1111/cei.12482
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
One among many factors involved in induction of rheumatoid arthritis (RA) are T cells, the differentiation of which depends upon a unique combination of stimulants and subsequent activation of diverse transcription factors. The aim of this study was to identify polymorphic variants in Smad3 and NFATc2 genes and their possible association with susceptibility to and severity of RA. A total of 272 RA patients, 321 for Smad3 and 304 for nuclear factor of activated T cells (NFAT)c2 healthy individuals, were examined for rs6494629 C/T and rs2289263 T/G Smad3 and rs880324 NFATc2 gene polymorphisms using the polymerase chain reaction-fragment length polymorphism (PCR-RFLP) method and TaqMan single nucleotide polymorphism (SNP) genotyping assay, respectively. Serum Smad3 and NFATc2 levels in RA patients and controls were measured by enzyme-linked immunosorbent assay (ELISA). The rs6494629 C/T Smad3 gene polymorphism under the recessive (TTversusCC+CT) and over-dominant (CC+TTversusCT) models were associated with RA (P=0014 and P=0008, respectively). Smad3 rs2289263 T/G revealed differences in the case-control distribution in co-dominant, recessive and over-dominant models (P=0037, P=0010, P=0034). Overall, rs6494629 C/T and rs2289263 T/G Smad3 gene polymorphisms were in a weak linkage disequilibrium (LD) with D=0116 and r(2)=0004. After Bonferroni correction, the genotype-phenotype analysis showed no significant correlation of the Smad3 rs6494629 C/T and rs2289263 T/G and NFATc2 rs2289263 TT polymorphisms with disease activity, joint damage and extra-articular manifestation in RA patients. Serum Smad3 and NFATc2 levels were significantly higher in RA patients than in control groups (both P=0 0000). The present findings indicated that Smad3 genetic polymorphisms may be associated with the susceptibility to RA in the Polish population.
引用
收藏
页码:444 / 453
页数:10
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