Expression of microRNA-23a-27a-24-2 cluster and its clinical significance in primary gout arthritis

Objective To investigate the role of microRNA(miR)-23a-27a-24-2 cluster in the patho-genesis of primary gout arthritis. Methods The subjects were divided into two groups: 55 acute gout patients (AG), and 35 healthy controls (HC). Clinical and laboratory parameters were collected. The expression level of miR-23a, miR-24-2, miR-27a was detected using real-time fluorescent quantitative polymerase chain reaction (PCR) (TaqMan probe). The PBMCs of HC were stimulated with 100 μg/ml for 12 h to intimate inflammatory environment, then to examine the expressions of miR-23a, miR-24-2, miR-27a in the cells. All features were analyzed by SPSS 17.0 statistical software, Wilcoxon rank sum test, t test and Spearman's correlations analysis were used for statistical analysis. Results ① The expression of miR-23a, miR-24-2, miR-27a in the group of AG [0.006(0.023), 0.986(1.313), 0.086(0.288)] was significantly lower than that in the HC group [0.180(0.629), 4.595 (4.273), 0.489(2.474)] and showed significant differences between the two groups (Z=-5.313, -3.108,-3.257; P<0.01, respectively). ② The expression of miR-23a, miR-24-2, miR-27a was positively correlated (r=0.548, r=0.690, r=0.523; P<0.01, respectively) in PBMCs of AG; in the AG patients, the level of miR-24-2 was positively correlated with total cholesterol, apolipoprotein B100 (r=0.46, r=0.44; P<0.05, respectively). ③ After 12 h induction, the expression of miR-23a, miR-24-2, miR-27a in monosodium urate group (0.002 6±0.000 4, 1.266 5±0.211 2, 0.043 4±0.002 8) was significantly lower than that in the control group (0.016 8±0.005 6, 1.625 6±0.263 4, 0.164 4±0.031 9) and showed significant difference between the two groups (t=-5.04, P<0.01; t=-2.61, P<0.05; t=-7.55, P<0.01). Conclusion The expression of miR-23a, miR-24-2, miR-27a in AG is significantly lower than that in the HC group and in vitro inflammatory environment. The results of this study suggest that these genes may participate the inflammatory autoimmune response as a negative regulator in gout, which may also be involved in regulating the lipid metabolism of gout. Key words: Arthritis, Gouty; MicroRNAs; miR-23a-27a-24-2 cluster