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MicroRNA‐29b regulates hypertrophy of murine mesenchymal stem cells induced toward chondrogenesis
Author(s) -
Zhao Chunrong,
Miao Ying,
Cao Zhen,
Shi Jian,
Li Jianmei,
Kang Fei,
Dou Ce,
Xie Zhao,
Xiang Qiang,
Dong Shiwu
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28161
Subject(s) - chondrogenesis , mesenchymal stem cell , microbiology and biotechnology , chondrocyte , muscle hypertrophy , antagomir , microrna , stem cell , chemistry , cartilage , biology , cancer research , endocrinology , anatomy , biochemistry , gene
Objective Chondrocyte hypertrophy, a terminal stage of chondrocyte differentiation, is essential to the endochondral bone formation and is one of the major pathological factors in osteoarthritis. This study investigated the role of microRNA‐29b (miR‐29b), which is involved in chondrogenesis, in the regulation of hypertrophy in chondrocytes. Methods miR‐29b expression was assessed during murine mesenchymal stem cells (mMSCs) chondrogenesis. To detect whether miR‐29b affects chondrocyte hypertrophy, the mMSCs induced toward chondrogenesis were transfected with miR‐29b or its antisense inhibitor (antagomiR‐29b). Finally, the differential effects of antagomiR‐29b on chondrocytes at different differentiation stages were evaluated by loss‐of‐function experiments. Results miR‐29b expression was low‐level during the early chondrogenic differentiation, however, it was changed to high level during hypertrophy. Subsequently, the gain‐of‐function and loss‐of‐function experiments had confirmed that miR‐29b promoted hypertrophy in mMSC‐derived chondrocytes. In addition, we confirmed that on day 7, when cells were treated with antagomiR‐29b, was the optimal intervention time for preventing hypertrophic phenotype of mMSCs in vitro. Conclusion miR‐29b regulated chondrogenesis homeostasis and enhance hypertrophic phenotype. These data suggest that miR‐29b is a key regulator of the chondrocyte phenotype derived from mMSCs and it might be a potential target for articular cartilage repair.