Open AccessNeural cell adhesion molecule regulates chondrocyte hypertrophy in chondrogenic differentiation and experimental osteoarthritis
Author(s) -
Cheng BinFeng,
Lian JunJiang,
Yang HaiJie,
Wang Lei,
Yu HaoHeng,
Bi JiaJia,
Gao YaoXin,
Chen SuJuan,
Wang Mian,
Feng ZhiWei
Publication year - 2020
Publication title -
stem cells translational medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.781
H-Index - 71
eISSN - 2157-6580
pISSN - 2157-6564
DOI - 10.1002/sctm.19-0190
Subject(s) - chondrogenesis , chondrocyte , mesenchymal stem cell , microbiology and biotechnology , neural cell adhesion molecule , cellular differentiation , muscle hypertrophy , chemistry , cartilage , medicine , biology , cell adhesion , cell , anatomy , biochemistry , gene
Chondrocyte hypertrophy‐like change is an important pathological process of osteoarthritis (OA), but the mechanism remains largely unknown. Neural cell adhesion molecule (NCAM) is highly expressed and involved in the chondrocyte differentiation of mesenchymal stem cells (MSCs). In this study, we found that NCAM deficiency accelerates chondrocyte hypertrophy in articular cartilage and growth plate of OA mice. NCAM deficiency leads to hypertrophic chondrocyte differentiation in both murine MSCs and chondrogenic cells, in which extracellular signal‐regulated kinase (ERK) signaling plays an important role. Moreover, NCAM expression is downregulated in an interleukin‐1β‐stimulated OA cellular model and monosodium iodoacetate‐induced OA rats. Overexpression of NCAM substantially inhibits hypertrophic differentiation in the OA cellular model. In conclusion, NCAM could inhibit hypertrophic chondrocyte differentiation of MSCs by inhibiting ERK signaling and reduce chondrocyte hypertrophy in experimental OA model, suggesting the potential utility of NCAM as a novel therapeutic target for alleviating chondrocyte hypertrophy of OA.