Y Liu1, X-L Zhang, X-F Li, Y-C Tang, X Zhao. 1. Department of Rheumatology, Qilu Hospital of Shandong University, Jinan, China. biyu20202719@163.com.
Abstract
OBJECTIVE: Several microRNAs have been reported to contribute the progression of rheumatoid arthritis (RA) due to the ectopic expression of miRNAs in fibroblast-like synoviocytes (FLS). However, the function of miR-212-3p in RA still has not been mentioned before. PATIENTS AND METHODS: We obtained serum, synovial tissues, and FLS samples from RA patients and normal donors. Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to analysis the expression level of miR-212-3p. By using miR-212-3p mimics and inhibitors, we detected the effects of miR-212-3p on cell proliferation, cell cycle, and apoptosis in RA-FLS. Dual-luciferase and Western-blot were employed to verify the target of miR-212-3p. In addition, we over-expressed the SOX5 in miR-212-3p mimics treatment FLS to emphasize our results. RESULTS: The level of miR-212-3p in serum, synovial tissues, and FLS from RA patients was lower than these in relative normal group. Up-regulation of miR-212-3p inhibited cell proliferation, promoted cell apoptosis; however, knockdown of miR-212-3p promoted cell growth but reduced cell apoptotic rate. Furthermore, we found SOX5 as a direct target of miR-212-3p in RA-FLS and up-regulation of SOX5 reversed the effects of miR-212-3p over-expression. CONCLUSIONS: miR-212-3p could reduce cell proliferation and promoted cell apoptosis of RA-FLS via repressing SOX5, which may provide a new biological target for RA treatment.
OBJECTIVE: Several microRNAs have been reported to contribute the progression of rheumatoid arthritis (RA) due to the ectopic expression of miRNAs in fibroblast-like synoviocytes (FLS). However, the function of miR-212-3p in RA still has not been mentioned before. PATIENTS AND METHODS: We obtained serum, synovial tissues, and FLS samples from RApatients and normal donors. Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to analysis the expression level of miR-212-3p. By using miR-212-3p mimics and inhibitors, we detected the effects of miR-212-3p on cell proliferation, cell cycle, and apoptosis in RA-FLS. Dual-luciferase and Western-blot were employed to verify the target of miR-212-3p. In addition, we over-expressed the SOX5 in miR-212-3p mimics treatment FLS to emphasize our results. RESULTS: The level of miR-212-3p in serum, synovial tissues, and FLS from RApatients was lower than these in relative normal group. Up-regulation of miR-212-3p inhibited cell proliferation, promoted cell apoptosis; however, knockdown of miR-212-3p promoted cell growth but reduced cell apoptotic rate. Furthermore, we found SOX5 as a direct target of miR-212-3p in RA-FLS and up-regulation of SOX5 reversed the effects of miR-212-3p over-expression. CONCLUSIONS:miR-212-3p could reduce cell proliferation and promoted cell apoptosis of RA-FLS via repressing SOX5, which may provide a new biological target for RA treatment.