Matrix metalloproteinase–9 promoter polymorphisms in Korean patients with systemic lupus erythematosus

SummaryTo investigate the association between functional promoter polymorphisms of matrix metalloproteinase–9 (MMP-9) and systemic lupus erythematosus (SLE), we analyzed MMP-9 promoter -1562 C>T and MMP-9 -90 (CA)n repeat polymorphisms in 135 Korean SLE patients (mean age, 34.7 years; 124 female and 11 male) and in 135 gender- and age-matched healthy controls (mean age, 35.4 years). Clinical and laboratory findings were collected during the follow-up period (mean, 63.5 months; range, 3–252 months), and Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Indexes were calculated. The levels of total MMP-9 were measured in sera of SLE patients and controls by enzyme-linked immunoabsorbent assay. The serum levels of MMP-9 in SLE patients were significantly lower than those of controls (mean ± standard error of the mean, 1421.6 ± 177.4 vs 3731.4 ± 441.4 ng/ml, p = 1.2×10−5 by t test). Both functional polymorphisms were under the Hardy-Weinberg equilibrium state except (CA)n repeat polymorphisms in SLE patients (p = 2.6×10−5 by χ2 goodness-of-fit test). The distribution of the MMP-9 promoter polymorphisms or haplotypes was not significantly different in SLE patients and controls. However the frequency of alleles with low numbers of CA repeats (n < 21, 11.9% vs 7.0%, p = 0.06 by the χ2 test; odds ratio = 1.78, 95% confidence interval = 0.99−3.20) and the prevalence of low CA repeats homozygote tended to be higher in patients than in controls (5.2% vs 0.7%, p = 0.07 by logistic regression, odds ratio = 7.29, 95% confidence interval = 0.88−60.10) in the recessive model. No relationship was found between MMP-9 polymorphisms and clinical features or damage as indicated by SLICC/ACR Damage Index in the study subjects. These results suggest that genetic polymorphisms of the MMP-9 promoter regions are not associated with the development of SLE in Korea.