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miR-17-5p Regulates Heterotopic Ossification by Targeting ANKH in Ankylosing Spondylitis
Xiong Qin1, Bo Zhu2, Tongmeng Jiang3
1Department of Bone and Soft Tissue, Affiliated Tumor Hospital of Guangxi Medical University, 530021 Nanning, China; Guangxi Engineering Center in Biomedical Materials for Tissue and Organ Regeneration, Guangxi Medical University, 530021 Nanning, China; Guangxi Collaborative Innovation Center for Biomedicine, Guangxi Medical University, 530021 Nanning, China.
Abstract:
Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized with heterotopic ossification of the axis joints ligaments, resulting in joint disability. MicroRNAs (miRNAs) are regulators of mRNAs that play a crucial role in the AS pathological process. Here, we showed that the level of miR-17-5p was significantly higher in fibroblasts and ligament tissues from AS patients as compared to the non-AS individuals. Knockdown of the miR-17-5p from the fibroblasts derived from AS patients exhibited decreased osteogenic differentiation and ossification. On the other hand, AS patient-derived fibroblasts overexpressing miR-17-5p displayed the increased osteogenesis. Furthermore, inhibition of miR-17-5p ameliorated osteophyte formation, and the sacroiliitis phenotype in AS rats received emulsified collagen. Mechanistically, miR-17-5p regulated osteogenic differentiation by targeting the 3' UTR of ankylosis protein homolog (ANKH). Also, downregulation of miR-17-5p slowed AS progression through regulation of cytokines, such as dickkopf-1 (DKK1) and vascular endothelial growth factor (VEGF). In conclusion, our findings reveal a role of the miR-17-5p-ANKH axis in the regulation of heterotopic ossification, which is essential for therapeutic intervention in heterotopic ossification in AS.
Insights
MicroRNAs (miRNAs) like miR-17-5p are key in ankylosing spondylitis (AS) bone growth. Targeting miR-17-5p may treat AS by reducing abnormal bone formation and inflammation.
Area of Science:
- Biochemistry
- Molecular Biology
- Rheumatology
Background:
- Ankylosing spondylitis (AS) is a chronic inflammatory condition leading to joint ossification and disability.
- MicroRNAs (miRNAs) are critical regulators in the pathological processes of AS.
Purpose of the Study:
- To investigate the role of miR-17-5p in the pathogenesis of ankylosing spondylitis.
- To explore the therapeutic potential of targeting miR-17-5p in AS.
Main Methods:
- Quantified miR-17-5p levels in AS patient tissues.
- Manipulated miR-17-5p expression in AS patient-derived fibroblasts.
- Assessed osteogenic differentiation and ossification in vitro and in vivo (AS rat model).
- Identified miR-17-5p targets, including ANKH, DKK1, and VEGF.
Main Results:
- miR-17-5p levels were significantly elevated in AS fibroblasts and ligament tissues.
- miR-17-5p knockdown reduced osteogenic differentiation and ossification in AS fibroblasts.
- Overexpression of miR-17-5p enhanced osteogenesis in AS fibroblasts.
- Inhibition of miR-17-5p ameliorated osteophyte formation and AS phenotypes in rats.
- miR-17-5p targets ANKH, DKK1, and VEGF, influencing osteogenesis and AS progression.
Conclusions:
- The miR-17-5p-ANKH axis is a key regulator of heterotopic ossification in AS.
- miR-17-5p plays a significant role in AS pathogenesis.
- Targeting miR-17-5p presents a potential therapeutic strategy for AS-related heterotopic ossification.
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