MicroRNA-124 involves in ankylosing spondylitis by targeting ANTXR2

Abstract

Objectives. A recent genome-wide association study or GWAS identified that anthrax roxin receptor 2 (ANTXR2) was one of the risk loci for ankylosing spondylitis (AS). Previous study also showed that ANTXR2 could potentially affect new bone formation. This study aimed to investigate the possible mechanisms of ANTXR2 involved in AS pathogenesis.

Methods. The expression level of ANTXR2 and miR-124 in peripheral blood was detected by quantitative real-time polymerase chain reaction or qRT-PCR. ANTXR2 was predicted to be a target gene of miR-124 by TargetScan, which was confirmed by luciferase reporter assays. Western blot analysis was used to further investigate the effect of miR-124 on c-Jun N-terminal kinase (JNK) activation and evaluate the activated status of autophagy.

Results. We evidenced that ANTXR2 was downregulated and miR-124 was upregulated in peripheral blood from AS patients. Intriguingly, miR-124 targeted ANTXR2 and overexpression of miR-124 in Jurkat cells notably inhibited ANTXR2 expression. ANTXR2 inhibition by miR-124 promoted JNK activation and induced autophagy.

Conclusions. Our results suggested that miR-124 might induce autophagy to participate in AS by targeting ANTXR2, which might be implicated in pathological process of AS.

Keywords:

• Ankylosing Spondylitis
• ANTXR2
• Autophagy
• JNK
• miR-124

Acknowledgments

This study was supported by grants from the National Natural Science Foundation of China (Grant Nos. 81001338 and 81201778) and the Promotive Research Fund for Excellent Young and Middle-aged Scientists of Shandong Province (Grant No. BS2011SW036).

Conflict of interest

None.