Human periodontal ligament stem cells (hPDLSCs) can undergo osteogenic differentiation under induction conditions. Cyclic tensile stress (CTS) can stimulate stem cell osteogenic differentiation. The present study explored the mechanism of CTS in hPDLSC osteogenic differentiation. The hPDLSCs of the 4th passage were selected. hPDLSCs were subjected to CTS with deformation of 10% elongation at 0.5 Hz for 1, 4, 8, 12 and 24 h. ALP activity and staining, ARS staining and detection of expressions of osteogenesis-related genes (RUNX2, OPN, Sp7 and OCN) were used to assess hPDLSC osteogenic differentiation ability. microRNA (miR)-129-5p and BMP2 expression and p-Smad1/5 level were detected under CTS stimulation. The binding relationship between miR-129-5p and BMP2 was predicted and verified. The osteogenic differentiation ability of CTS-treated hPDLSCs was evaluated after intervention of miR-129-5p and BMP2. CTS induced hPDLSC osteogenic differentiation, as manifested by increased ALP activities, osteogenesis-related gene expressions and mineralized nodules, together with positive ALP staining. CTS inhibited miR-129-5p expression, and promoted BMP2 expression and p-Smad1/5 level in hPDLSCs. miR-129-5p targeted BMP2. Overexpressed miR-129-5p or silenced BMP2 prevented hPDLSC osteogenic differentiation ability. We demonstrated that CTS inhibited miR-129-5p expression, and then activated the BMP2/Smad pathway, thereby showing stimulative effects on hPDLSC osteogenic differentiation.

人牙周膜干细胞 (hPDLSCs) 可以在诱导条件下进行成骨分化。循环拉伸应力（CTS）可以刺激干细胞成骨分化。本研究探讨了CTS在hPDLSC成骨分化中的作用机制。选择第4代的hPDLSC。hPDLSCs 在 0.5 Hz 下以 10% 的伸长率变形 1、4、8、12 和 24 小时进行 CTS。采用ALP活性及染色、ARS染色及成骨相关基因（RUNX2、OPN、Sp7和OCN）表达检测hPDLSC成骨分化能力。在 CTS 刺激下检测 microRNA (miR)-129-5p 和 BMP2 表达和 p-Smad1/5 水平。预测并验证了miR-129-5p与BMP2的结合关系。在 miR-129-5p 和 BMP2 干预后评估 CTS 处理的 hPDLSCs 的成骨分化能力。CTS 诱导 hPDLSC 成骨分化，表现为 ALP 活性增加、成骨相关基因表达和矿化结节，以及 ALP 染色阳性。CTS 抑制 miR-129-5p 表达，并促进 hPDLSCs 中 BMP2 表达和 p-Smad1/5 水平。miR-129-5p 靶向 BMP2。过表达的 miR-129-5p 或沉默的 BMP2 阻止了 hPDLSC 成骨分化能力。我们证明 CTS 抑制 miR-129-5p 表达，然后激活 BMP2/Smad 通路，从而显示对 hPDLSC 成骨分化的刺激作用。成骨相关基因表达和矿化结节，以及阳性 ALP 染色。CTS 抑制 miR-129-5p 表达，并促进 hPDLSCs 中 BMP2 表达和 p-Smad1/5 水平。miR-129-5p 靶向 BMP2。过表达的 miR-129-5p 或沉默的 BMP2 阻止了 hPDLSC 成骨分化能力。我们证明 CTS 抑制 miR-129-5p 表达，然后激活 BMP2/Smad 通路，从而显示对 hPDLSC 成骨分化的刺激作用。成骨相关基因表达和矿化结节，以及阳性 ALP 染色。CTS 抑制 miR-129-5p 表达，并促进 hPDLSCs 中 BMP2 表达和 p-Smad1/5 水平。miR-129-5p 靶向 BMP2。过表达的 miR-129-5p 或沉默的 BMP2 阻止了 hPDLSC 成骨分化能力。我们证明 CTS 抑制 miR-129-5p 表达，然后激活 BMP2/Smad 通路，从而显示对 hPDLSC 成骨分化的刺激作用。