| ORIGINAL ARTICLE |
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| Year : 2016 | Volume
: 11
| Issue : 2 | Page : 78-81 |
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STAT4 rs7574865 polymorphism in Iranian patients with rheumatoid arthritis
Zeinab Alizadeh1, Ali Farazmand2, Maassoomeh Akhlaghi3, Ahmad Reza Jamshidi3, Abtin Shahlaee3, Jafar Karami3, Elmira Shamsian3, Mahdi Mahmoudi3
1 Rheumatology Research Center, Tehran University of Medical Sciences; Department of Cell and Molecular Biology, University of Tehran, Tehran, Iran
2 Department of Cell and Molecular Biology, University of Tehran, Tehran, Iran
3 Rheumatology Research Center, Tehran University of Medical Sciences, Tehran, Iran
Correspondence Address:
Mahdi Mahmoudi
Rheumatology Research Center, Tehran University of Medical Sciences, Tehran
Iran
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.1016/j.injr.2016.02.002
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Objectives: The gene encoding signal transducer and activator of transcription 4 (STAT4) has been documented to be associated with rheumatoid arthritis (RA) in several populations. The aim of this study was to determine the association of the STAT4 gene polymorphism (rs7574865) with RA in the Iranian population.
Methods: This study included 612 Iranian RA patients and 389 healthy control subjects. For all samples, DNA was genotyped for STAT4 G>T (rs7574865) polymorphism using the MGB TaqMan Allelic Discrimination method.
Results: In our survey, the frequencies of GG, GT, and TT genotypes were 50%, 41.3%, and 8.7% in RA patients, and 51.4%, 37.5%, and 11.1% in controls (P > 0.05), respectively. STAT4 rs7574865 alleles were not associated with the disease risk in the Iranian population (P > 0.05).
Conclusions: Although most studies have proposed STAT4 polymorphisms as a susceptible risk factor for RA, we did not detect any significant association between the STAT4 polymorphism and RA in our study. Population-based studies help to identify genetic determinants of disease susceptibility. Possible explanations for differences in susceptible genetic factors among populations could be different genetic predispositions and contribu- tion of gene-gene or gene-environment interactions. |
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