Author:
Tu Manli,Yang Mi,Yu Nanxi,Zhen Gehua,Wan Mei,Liu Wenlong,Ji Baochao,Ma Hairong,Guo Qiaoyue,Tong Peijian,Cao Li,Luo Xianghang,Cao Xu
Abstract
Abstract
Osteoarthritis (OA) causes the destruction of joints. Its pathogenesis is still under investigation, and there is no effective disease-modifying therapy. Here, we report that elevated cyclooxygenase-2 (COX-2) expression in the osteocytes of subchondral bone causes both spontaneous OA and rheumatoid arthritis (RA). The knockout of COX-2 in osteocytes or treatment with a COX-2 inhibitor effectively rescues the structure of subchondral bone and attenuates cartilage degeneration in spontaneous OA (STR/Ort) mice and tumor necrosis factor-α transgenic RA mice. Thus, elevated COX-2 expression in subchondral bone induces both OA-associated and RA-associated joint cartilage degeneration. The inhibition of COX-2 expression can potentially modify joint destruction in patients with arthritis.
Funder
U.S. Department of Health & Human Services | NIH | National Institute of Arthritis and Musculoskeletal and Skin Diseases
Publisher
Springer Science and Business Media LLC
Subject
Physiology,Histology,Endocrinology, Diabetes and Metabolism
Cited by
35 articles.
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