Osteoclast-associated receptor blockade prevents articular cartilage destruction via chondrocyte apoptosis regulation

Doo Ri Park, Jihee Kim, Gyeong Min Kim, Haeseung Lee, Minhee Kim, Donghyun Hwang, Hana Lee, Han-Sung Kim, Wankyu Kim, Min Chan Park, Hyunbo Shim and Soo Young Lee ()
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Doo Ri Park: Ewha Womans University
Jihee Kim: Ewha Womans University
Gyeong Min Kim: Ewha Womans University
Haeseung Lee: Ewha Womans University
Minhee Kim: Ewha Womans University
Donghyun Hwang: Yonsei University
Hana Lee: Yonsei University
Han-Sung Kim: Yonsei University
Wankyu Kim: Ewha Womans University
Min Chan Park: Yonsei University College of Medicine
Hyunbo Shim: Ewha Womans University
Soo Young Lee: Ewha Womans University

Nature Communications, 2020, vol. 11, issue 1, 1-11

Abstract: Abstract Osteoarthritis (OA), primarily characterized by articular cartilage destruction, is the most common form of age-related degenerative whole-joint disease. No disease-modifying treatments for OA are currently available. Although OA is primarily characterized by cartilage destruction, our understanding of the processes controlling OA progression is poor. Here, we report the association of OA with increased levels of osteoclast-associated receptor (OSCAR), an immunoglobulin-like collagen-recognition receptor. In mice, OSCAR deletion abrogates OA manifestations, such as articular cartilage destruction, subchondral bone sclerosis, and hyaline cartilage loss. These effects are a result of decreased chondrocyte apoptosis, which is caused by the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in induced OA. Treatments with human OSCAR-Fc fusion protein attenuates OA pathogenesis caused by experimental OA. Thus, this work highlights the function of OSCAR as a catabolic regulator of OA pathogenesis, indicating that OSCAR blockade is a potential therapy for OA.

Date: 2020
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DOI: 10.1038/s41467-020-18208-y

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