Polymorphism and protein expression of MUTYH gene for risk of rheumatoid arthritis.
We have previously described the association between rheumatoid arthritis (RA) prevalence and the two mutY Homolog (E. coli) (MUTYH) SNPs (rs3219463 and rs3219476) among the Taiwanese population. This present study will aim to elucidate whether the SNPs can alter the expression of EGFR in the progression of RA.



The cohort study included 368 Taiwan's Han Chinese RA patients and 364 healthy controls. Blood samples collected from the participants were analyzed to determine their serum MUTYH levels and to identify rs3219463 SNP of MUTYH from their genomic DNA.



Our data resulted in a statistically significant difference in genotype frequency distributions at rs3219463 for RA patients and controls (p < 0.0002). Also, the patients with G carrier at rs3219463 were less likely to suffer from painful joints (p < 0.006) and DAS28 scores (p < 0.003). Furthermore, the increase in serum level of MUTYH was also observed in RA patients (p < 0.005).



Our study showed that RA is associated with rs3219463 SNP in EGFR gene and an increased serum level of the MUTYH protein. These findings suggest MUTYH is worthy of further investigation as a therapeutic target for RA.
School of Chinese Medicine, China Medical University, Taichung, 404, Taiwan.|Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404, Taiwan.
Shih-Yin
SY
Chen
Division of Plastic and Reconstructive Surgery, China Medical University Hospital, Taichung, 404, Taiwan.
Hsin-Han
HH
Chen
School of Chinese Medicine, China Medical University, Taichung, 404, Taiwan.|Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404, Taiwan.
Yu-Chuen
YC
Huang
Center for Neuropsychiatry, China Medical University Hospital, Taichung, 404, Taiwan.
Shih-Ping
SP
Liu
School of Chinese Medicine, China Medical University, Taichung, 404, Taiwan.|Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404, Taiwan.
Ying-Ju
YJ
Lin
Department of Physical Medicine and Rehabilitation, China Medical University Hospital, Taichung, 404, Taiwan.
Sui-Foon
SF
Lo
Department of Microbiology and Immunology, and Institute of Microbiology and Immunology, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Yuan-Yen
YY
Chang
Department of Optometry, Asia University, Taichung, 413, Taiwan.
Hui-Wen
HW
Lin
School of Chinese Medicine, China Medical University, Taichung, 404, Taiwan. hcm.jeffrey@msa.hinet.net.|Division of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, 404, Taiwan. hcm.jeffrey@msa.hinet.net.
Chung-Ming
CM
Huang
Genetics Center, Department of Medical Research, China Medical University Hospital, Taichung, 404, Taiwan. d0704@mail.cnuh.org.tw.|Department of Pediatrics, China Medical University Hospital, Taichung, 404, Taiwan. d0704@mail.cnuh.org.tw.|Department of Medical Genetics, China Medical University Hospital, Taichung, 404, Taiwan. d0704@mail.cnuh.org.tw.
Fuu-Jen
FJ
Tsai
D001172:Arthritis, Rheumatoid / Q000097:blood / Q000175:diagnosis* / Q000235:genetics*; D015331:Cohort Studies; D045647:DNA Glycosylases / Q000097:blood / Q000235:genetics*; D005260:Female; D015870:Gene Expression; D020022:Genetic Predisposition to Disease / Q000453:epidemiology / Q000235:genetics*; D006801:Humans; D008297:Male; D010865:Pilot Projects; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D012307:Risk Factors
D045647:DNA Glycosylases; C061738:mutY adenine glycosylase
CNVs; MUTYH; Oxidative DNA damage. DAS28; RA; SNPs