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Osteoclast-derived DEL1 promotes pathological bone formation in ankylosing spondylitis by regulating RUNX2 expression
Seung Hoon Lee1, Chanhyeok Jeon1, Dongju Kim1
1Hanyang University Institute for Rheumatology Research (HYIRR), Hanyang University, Seoul, 04763, South Korea.
Differentiation; Research in Biological Diversity
|May 13, 2026
Summary
Developmental endothelial locus-1 (DEL1) drives new bone formation in ankylosing spondylitis (AS). Targeting the DEL1-integrin αVβ3-RUNX2 pathway may prevent spinal damage in AS patients.
Area of Science:
- Immunology
- Bone Biology
- Rheumatology
Background:
- Ankylosing spondylitis (AS) is a chronic inflammatory condition marked by abnormal bone growth.
- The role of developmental endothelial locus-1 (DEL1) in AS pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the role of DEL1 in new bone formation in AS.
- To determine the association between DEL1 and spinal progression in AS patients.
Main Methods:
- Measured DEL1 levels in AS patients and in vitro models.
- Treated human osteoblast precursors with DEL1 and an integrin inhibitor.
- Utilized a mouse model of AS, administering DEL1 or inhibitor, followed by micro-CT and histological analysis.
Main Results:
- DEL1 expression increased with osteoclast differentiation and correlated with AS disease progression in mice.
- Plasma DEL1 levels correlated with structural damage in AS patients.
- DEL1 promoted osteoblast differentiation and mineralization, effects blocked by an integrin inhibitor.
Conclusions:
- DEL1 is an osteoclast-derived factor promoting new bone formation in AS.
- DEL1 signaling via integrin αVβ3-RUNX2 axis drives pathological bone formation.
- Targeting this pathway offers a potential strategy to prevent AS structural damage.
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