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The complement factor H-related protein-5 (CFHR5) exacerbates pathological bone formation in ankylosing spondylitis
Ji-Hyun Lee1,2, Seung Hoon Lee3, Chanhyeok Jeon3
1Department of Rheumatology, Eulji Rheumatology Research Institute, Eulji University School of Medicine, 712 Dongil-Ro, Uijeongbu, Gyeonggi-Do, 11759, Republic of Korea.
Journal of Molecular Medicine (Berlin, Germany)
|February 28, 2024
Summary
Complement factor H-related protein-5 (CFHR5) is elevated in ankylosing spondylitis (AS) and exacerbates pathological bone formation. Targeting CFHR5 may offer a new therapeutic strategy for AS patients.
Area of Science:
- Rheumatology
- Immunology
- Bone Biology
Background:
- Ankylosing spondylitis (AS) is a chronic inflammatory disease marked by excessive new bone formation.
- Complement factor H-related protein-5 (CFHR5) is elevated in AS patients.
- The role of CFHR5 in AS pathogenesis, particularly new bone formation, is not fully understood.
Purpose of the Study:
- To investigate the role of CFHR5 in the pathological bone formation associated with ankylosing spondylitis.
- To explore the relationship between CFHR5, proinflammatory cytokines, and C-reactive protein (CRP) in AS.
- To determine the effect of CFHR5 on osteoprogenitors and ectopic bone formation in AS models.
Main Methods:
- Quantified serum levels of CFHR5 and proinflammatory cytokines (TNF, IL-6, IL-17A, IL-23) in AS patients and healthy controls (HC).
- Analyzed correlations between CFHR5, cytokines, and CRP.
- Administered recombinant CFHR5 in a mouse model of AS (curdlan-injected SKG) and assessed bone formation via micro-CT.
- Examined CFHR5 expression in AS-derived osteoprogenitors and its effect on osteogenic differentiation and mineralization in vitro, including MMP13 expression.
Main Results:
- CFHR5 and proinflammatory cytokines were elevated in AS patients compared to HC.
- CFHR5 levels positively correlated with high CRP but not significantly with proinflammatory cytokines in AS.
- In vivo, CFHR5 treatment increased ectopic bone formation in the ankle joints of AS model mice.
- In vitro, CFHR5 upregulated basal expression in AS-osteoprogenitors and enhanced bone mineralization during osteogenic differentiation, accompanied by increased MMP13 expression.
Conclusions:
- CFHR5 is upregulated in AS and contributes to pathological bone formation.
- CFHR5 exacerbates ectopic bone formation and enhances osteoprogenitor mineralization in AS.
- Therapeutic targeting of CFHR5 presents a potential strategy for treating ankylosing spondylitis.
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