期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 120, 期 5, 页码 8742-8753出版社
WILEY
DOI: 10.1002/jcb.28161
关键词
chondrocyte hypertrophy; chondrogenesis; mesenchymal stem cells; microRNA-29b
资金
- National Key Technology Research and Development Program of China [2017YFC1103300]
- Nature Science Foundation of China [31870962, 81571893]
- Major project of Logistics Research Plan of PLA [AWS17J004]
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.
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