@article {Huang1104, author = {Chun-Huang Huang and James Cheng-Chung Wei and Wei-Chiao Chang and Shang-Yan Chiou and Chia-Hsuan Chou and Yu-Jie Lin and Pei-Hsuan Hung and Ruey-Hong Wong}, title = {Higher Expression of Whole Blood MicroRNA-21 in Patients with Ankylosing Spondylitis Associated with Programmed Cell Death 4 mRNA Expression and Collagen Cross-linked C-telopeptide Concentration}, volume = {41}, number = {6}, pages = {1104--1111}, year = {2014}, doi = {10.3899/jrheum.130515}, publisher = {The Journal of Rheumatology}, abstract = {Objective. Bone loss is a recognized feature of ankylosing spondylitis (AS). The binding of microRNA-21 (miR-21) to programmed cell death 4 (PDCD4) could inhibit the expression of PDCD4 and further induce the activation of osteoclasts. In the present study, we compared the difference in miR-21 expression between patients with AS and healthy controls, and evaluated the relationships of miR-21, PDCD4 mRNA, and bone erosion in patients with AS. The influences of nonsteroidal antiinflammatory drugs (NSAID) and disease-modifying antirheumatic drugs (DMARD) on the expressions of miR-21 and PDCD4 mRNA in patients with AS were also assessed. Methods. Whole blood miR-21 and PDCD4 mRNA expression were evaluated by quantitative real-time PCR among 122 patients with AS and 122 healthy controls. The serum level of collagen cross-linked C-telopeptide (CTX) was measured using ELISA. Results. When compared to controls, patients with AS had significantly higher levels of miR-21, PDCD4 mRNA, and CTX. MiR-21 expression was negatively correlated with PDCD4 mRNA expression in patients with AS who were taking neither NSAID nor DMARD. Interestingly, significantly positive correlations between miR-21 expression with PDCD4 mRNA expression (r = 0.33, p = 0.01) and CTX level (r = 0.44, p \< 0.01) were observed in patients with AS who were taking sulfasalazine. Positive correlations of miR-21 and CTX level were also observed in AS patients with disease duration \< 7.0 years (r = 0.36, p = 0.004) and active disease (r = 0.42, p = 0.001). Conclusion. The expression of miR-21 might have a role in the development of AS.}, issn = {0315-162X}, URL = {https://www.jrheum.org/content/41/6/1104}, eprint = {https://www.jrheum.org/content/41/6/1104.full.pdf}, journal = {The Journal of Rheumatology} }