期刊
JOURNAL OF BONE AND MINERAL RESEARCH
卷 37, 期 10, 页码 1944-1955出版社
WILEY
DOI: 10.1002/jbmr.4661
关键词
CCN2; IL-17; MIR-655; OSTEOCLASTS; ILK; SYK
资金
- Taiwan's Ministry of Science and Technology [MOST 108-2320-B-039-064, MOST 110-2320-B-039-022-MY3, MOST 110-2314-B-039-008, MOST 110-2314-B-039-012, MOST 111-2314-B-039-051]
- China Medical University Beigang Hospital [110CMUBHR-07, CMUBHR-109-011]
- China Medical University Hospital [DMR-110-074, DMR-111-235, DMR-111-078]
- China Medical University [CMU 110-MF-11]
Osteoarthritis is associated with upregulation of CCN2 and IL-17 expression, with CCN2 promoting IL-17 synthesis and osteoclast formation, and affecting IL-17 production by reducing miR-655 expression.
Osteoarthritis (OA) is associated with extensive upregulation of osteoclastogenesis and subsequent bone breakdown. The CCN family protein connective tissue growth factor (CCN2, also called CCN2) enhances inflammatory cytokine production in OA disease. The cytokine interleukin (IL)-17 is known to induce osteoclastogenesis and bone erosion in arthritic disease. Our retrieval of data from the Gene Expression Omnibus (GEO) data set and clinical tissues exhibited higher CCN2 and IL-17 expression in OA synovial sample than in normal healthy samples. We observed the same phenomenon in synovial tissue from rats with anterior cruciate ligament transaction (ACLT)-elicited OA compared with synovial tissue from control healthy rats. We also found that CCN2 facilitated increases in IL-17 synthesis in human OA synovial fibroblasts (OASFs) and promoted osteoclast formation. CCN2 affected IL-17 production by reducing miR-655 expression through the ILK and Syk signaling cascades. Our findings improve our understanding about the effect of CCN2 in OA pathogenesis and, in particular, IL-17 production and osteoclastogenesis, which may help with the design of more effective OA treatments. (c) 2022 American Society for Bone and Mineral Research (ASBMR).
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