한빛사논문
- 조회1,503
Doo Ri Park1,2, Jihee Kim1,2, Gyeong Min Kim1,2, Haeseung Lee1, Minhee Kim1,2, Donghyun Hwang3, Hana Lee3, Han-Sung Kim3, Wankyu Kim1, Min Chan Park4, Hyunbo Shim1 & Soo Young Lee1,2,*
1Department of Life Science, Ewha Womans University, Seoul 03760, South Korea.
2The Research Center for Cellular Homeostasis, Ewha Womans University, Seoul 03760, South Korea.
3Department of Biomedical Engineering, Yonsei University, Wonju 26493, South Korea.
4Division of Rheumatology, Department of Internal Medicine, Yonsei University College of Medicine, Seoul 06273, South Korea.
*Corresponding author
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.
논문정보
- Research article
- 2020년 08월 (BRIC 등록일 2020-09-04)
- 국내 연구진
- 생명과학 > 면역학
댓글 작성 로그인
팝업 닫기관련 링크
소속기관 논문보기
관련분야 논문보기
해당논문 저자보기
