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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.
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.
Background: MicroRNAs (miRNAs) are a class of small non-coding RNA molecules that regulate gene expression. There is increasing evidence that some miRNAs are involved in the pathology of diabetes mellitus (DM) and its complications. We hypothesized that the functions of certain miRNAs and the changes in their patterns of expression may contribute to the pathogenesis of impaired fractures due to DM. Methods: In this study, 108 male Sprague-Dawley rats were divided into DM and control groups. DM rats were created by a single intravenous injection of streptozotocin. Closed transverse femoral shaft fractures were created in both groups. On post-fracture days 5, 7, 11, 14, 21, and 28, miRNA was extracted from the newly generated tissue at the fracture site. Microarray analysis was conducted with miRNA samples from each group on post-fracture days 5 and 11. The microarray findings were validated by real-time polymerase chain reaction (PCR) analysis at each time point. Results: Microarray analysis revealed that, on days 5 and 11, 368 and 207 miRNAs, respectively, were upregulated in the DM group, compared with the control group. The top four miRNAs on day 5 were miR-339-3p, miR451-5p, miR-532-5p, and miR-551b-3p. The top four miRNAs on day 11 were miR-221-3p, miR376a-3p, miR-379-3p, and miR-379-5p. Among these miRNAs, miR-221-3p, miR-339-3p, miR-376a-3p, miR-379-5p, and miR-451-5p were validated by real-time PCR analysis. Furthermore, PCR analysis revealed that these five miRNAs were differentially expressed with dynamic expression patterns during fracture healing in the DM group, compared with the control group. Conclusions: Our findings will aid in understanding the pathology of impaired fracture healing in DM and may support the development of molecular therapies using miRNAs for the treatment of impaired fracture healing in patients with DM.
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