IgSF11 deficiency alleviates osteoarthritis in mice by suppressing early subchondral bone changes

Osteoarthritis (OA) is a degenerative joint disease. While it is classically characterized by articular cartilage destruction, OA affects all tissues in the joints and is thus also accompanied by local inflammation, subchondral bone changes, and persistent pain. However, our understanding of the und...

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Published inExperimental & molecular medicine Vol. 55; no. 12; pp. 2576 - 2585
Main Authors Kim, Gyeong Min, Kim, Jihee, Lee, June-Yong, Park, Min-Chan, Lee, Soo Young
Format Journal Article
LanguageEnglish
Published United States Springer Nature B.V 01.12.2023
Nature Publishing Group
생화학분자생물학회
Subjects
Animal models
Animals
Arthritis
Artificial intelligence
Bone and Bones
Bone remodeling
Bone resorption
Bone Resorption - genetics
Cartilage
Cartilage diseases
Cartilage, Articular
Cell differentiation
Disease Models, Animal
Immunoglobulins
Joint diseases
Meniscus
Mice
Osteoarthritis
Osteoarthritis - complications
Osteoarthritis - genetics
Osteoclastogenesis
Osteoclasts
Subchondral bone
생화학
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Summary:Osteoarthritis (OA) is a degenerative joint disease. While it is classically characterized by articular cartilage destruction, OA affects all tissues in the joints and is thus also accompanied by local inflammation, subchondral bone changes, and persistent pain. However, our understanding of the underlying subchondral bone dynamics during OA progression is poor. Here, we demonstrate the contribution of immunoglobulin superfamily 11 (IgSF11) to OA subchondral bone remodeling by using a murine model. In particular, IgSF11 was quickly expressed by differentiating osteoclasts and upregulated in subchondral bone soon after destabilization-of-the-medial-meniscus (DMM)-induced OA. In mice, IgSF11 deficiency not only suppressed subchondral bone changes in OA but also blocked cartilage destruction. The IgSF11-expressing cells in OA subchondral bone were found to be involved in osteoclast maturation and bone resorption and colocalized with receptor-activator of nuclear-factor κ-B (RANK), the key osteoclast differentiation factor. Thus, our study shows that blocking early subchondral bone changes in OA can ameliorate articular cartilage destruction in OA.
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ISSN:2092-6413
1226-3613
2092-6413
DOI:10.1038/s12276-023-01126-6