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2010 | 51 | 4 |

Tytuł artykułu

Genetic polymorphisms of the DNA repair gene MPG may be associated with susceptibility to rheumatoid arthritis

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
Rheumatoid arthritis (RA) is a chronic autoimmune disease and can lead to deformities and severe disabilities, due to irreversible damage of tendons, joints, and bones. A previous study indicated that a DNA repair system was involved in the development of RA. In this study, we investigated the association of four N-methylpurine-DNA glycosylase (MPG) gene polymorphisms (rs3176364, rs710079, rs2858056, and rs2541632) with susceptibility to RA in 384 Taiwanese individuals (192 RA patients and 192 control subjects). Our data show a statistically significant difference in genotype frequency distributions at rs710079 and rs2858056 SNPs between RA patients and control groups (P = 0.040 and 0.029, respectively). Our data also indicated that individuals with the GG genotype at rs2858056 SNP may have a higher risk of developing RA. In addition, compared with the haplotype frequencies between case and control groups, individuals with the GCGC haplotype appeared to be at a greater risk of RA progression (P = 0.003, OR = 1.75; 95% CI = 1.20-1.55). Our results suggest that rs710079 and rs2858056 polymorphisms and the GCGC haplotype in the MPG gene are associated with the risk of RA progression, and thus may be used as molecular markers of RA if they are confirmed by further research.

Wydawca

-

Rocznik

Tom

51

Numer

4

Opis fizyczny

p.519-521,fig.,ref.

Twórcy

autor
  • Genetic Center, Department of Medical Research, China Medical University Hospital, No. 2 Yuh Der Road, Taichung, Taiwan
  • Graduate Institute of Chinese Medical Science, College of Chinese Medicine, Taichung, Taiwan
autor
  • Genetic Center, Department of Medical Research, China Medical University Hospital, No. 2 Yuh Der Road, Taichung, Taiwan
  • Graduate Institute of Chinese Medical Science, College of Chinese Medicine, Taichung, Taiwan
autor
  • Division of Immunology and Rheumatology, Taichung, Taiwan
autor
  • Genetic Center, Department of Medical Research, China Medical University Hospital, No. 2 Yuh Der Road, Taichung, Taiwan
  • Graduate Institute of Chinese Medical Science, College of Chinese Medicine, Taichung, Taiwan
autor
  • Genetic Center, Department of Medical Research, China Medical University Hospital, No. 2 Yuh Der Road, Taichung, Taiwan
  • Graduate Institute of Chinese Medical Science, College of Chinese Medicine, Taichung, Taiwan
autor
  • Genetic Center, Department of Medical Research, China Medical University Hospital, No. 2 Yuh Der Road, Taichung, Taiwan
  • Graduate Institute of Chinese Medical Science, College of Chinese Medicine, Taichung, Taiwan
autor
  • Center for Neuropsychiatry, Taichung, Taiwan
autor
  • Department of Health Risk Management Taichung, Taiwan
autor
  • Department of Microbiology, School of Medicine Taichung, Taiwan
autor
  • Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan
autor
  • Graduate Institute of Chinese Medical Science, College of Chinese Medicine, Taichung, Taiwan
autor
  • Genetic Center, Department of Medical Research, China Medical University Hospital, No. 2 Yuh Der Road, Taichung, Taiwan
  • Department of Medical Genetics, China Medical University Hospital, Taichung, Taiwan

Bibliografia

  • Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, Cooper NS, et al. 1988. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 31: 315-324.
  • Feldmann M, Brennan FM, Maini RN, 1996. Rheumatoid arthritis. Cell 85: 307-310.
  • Harris ED Jr, 1990. Rheumatoid arthritis. Pathophysiology and implications for therapy. N Engl J Med 322:1277-1289.
  • Lynn AH, Kwoh CK, Venglish CM, Aston CE, Chakravarti A, 1995. Genetic epidemiology of rheumatoid arthritis. Am J Hum Genet 57: 150-159.
  • Shao L, Fujii H, Colmegna I, Oishi H, Goronzy JJ, Weyand CM, 2009. Deficiency of the DNA repair enzyme ATM in rheumatoid arthritis. J Exp Med 206: 1435-49.
  • Weyand CM, Klimiuk PA, Goronzy JJ, 1998. Heterogeneity of rheumatoid arthritis: from phenotypes to genotypes. Springer Semin Immunopathol 20: 5-22.
  • Yamada R, Ymamoto K, 2005. Recent findings on genes associated with inflammatory disease. Mutat Res 573: 136-151.
  • Ziff M, 1990. Rheumatoid arthritis-its present and future. J Rheumatol 17: 127-133.

Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

bwmeta1.element.dl-catalog-87802a4b-22e9-48ae-bd42-2f05b645c202
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