人骨髓间充质干细胞（hBMMSCs）是骨工程的有希望的细胞来源，因为它们具有高分化成成骨细胞的潜力。本研究的目标是评估微RNA-126（miR-126）并检查其对hBMMSCs的成骨分化的影响。在本研究中，我们调查miR-126在成骨分化进程中以及在OD诱导期间hBMMSCs的凋亡和炎症中的作用。OD在hBMMSCs中被诱导，通过Alizarin Red S（AR）染色和定量PCR（qPCR）评估基质矿化及其他OD相关标记。进行增加-和失去功能研究以证明miR-126在hBMMSCs的OD中的作用。流式细胞术和基于qPCR的细胞因子表达研究用于研究miR-126对hBMMSCs的凋亡和炎症的影响。结果表明，在hBMMSCs的OD期间，miR-126表达下调。增加-和失去功能检测揭示miR-126升高能抑制hBMMSCs的分化成成骨细胞，而miR-126表达下调则促进分化，这一点可以通过确定成骨基因和碱性磷酸酶活性来评估。此外，miR-126水平与炎症因子的产生和凋亡细胞死亡呈正相关。此外，我们的结果表明，miR-126不仅负调节B细胞淋巴瘤2（Bcl-2）的表达，还抑制细胞外信号调节蛋白激酶（ERK）1 / 2的磷酸化。此外，恢复ERK1 / 2的活性和上调Bcl-2的表达都能抵消miR-126介导的hBMMSCs OD抑制，通过促进炎症和凋亡反应，使得骨生长得以促进。总之，我们的发现揭示了与hBMMSCs成骨细胞分化相关的新型分子机制，这有望通过对抗miR-126介导的ERK1 / 2活性和Bcl-2表达抑制来促进骨形成。

Human bone marrow mesenchymal stem cells (hBMMSCs) are a promising cell source for bone engineering owing to their high potential to differentiate into osteoblasts. The objective of the present study is to assess microRNA-126 (miR-126) and examine its effects on the osteogenic differentiation of hBMMSCs. In this study, we investigate the role of miR-126 in the progression of osteogenic differentiation (OD) as well as the apoptosis and inflammation of hBMMSCs during OD induction. OD is induced in hBMMSCs, and matrix mineralization along with other OD-associated markers are evaluated by Alizarin Red S (AR) staining and quantitative PCR (qPCR). Gain- and loss-of-function studies are performed to demonstrate the role of miR-126 in the OD of hBMMSCs. Flow cytometry and qPCR-based cytokine expression studies are performed to investigate the effect of miR-126 on the apoptosis and inflammation of hBMMSCs. The results indicate that miR-126 expression is downregulated during the OD of hBMMSCs. Gain- and loss-of function assays reveal that miR-126 upregulation inhibits the differentiation of hBMMSCs into osteoblasts, whereas the downregulation of miR-126 promotes hBMMSC differentiation, as assessed by the determination of osteogenic genes and alkaline phosphatase activity. Furthermore, the miR-126 level is positively correlated with the production of inflammatory cytokines and apoptotic cell death. Additionally, our results suggest that miR-126 negatively regulates not only B-cell lymphoma 2 (Bcl-2) expression but also the phosphorylation of extracellular signal‑regulated protein kinase (ERK) 1/2. Moreover, restoring ERK1/2 activity and upregulating Bcl-2 expression counteract the miR-126-mediated suppression of OD in hBMMSCs by promoting inflammation and apoptosis, respectively. Overall, our findings suggest a novel molecular mechanism relevant to the differentiation of hBMMSCs into osteoblasts, which can potentially facilitate bone formation by counteracting miR-126-mediated suppression of ERK1/2 activity and Bcl-2 expression.