AimTo investigate the role of lncRNA Lockd in mandibular mesenchymal stem cell (M‐MSC) proliferation and osteogenic capability in the inflammatory microenvironment, focusing on its interaction with SUZ12.Materials and MethodsUsing lncR Lockd knockdown/overexpression cell models and a murine periodontitis model, we explored Lockd's effects on M‐MSC proliferation and osteogenic capability in the inflammatory microenvironment. Predictions from multiple databases and a series of rescue experiments revealed the regulatory role of the Lockd/SUZ12 signalling axis of M‐MSC in the inflammatory microenvironment.ResultsLockd was found to stimulate M‐MSC proliferation but impair osteogenic differentiation. The in vitro studies suggested that the activation of Lockd negatively inhibited the osteogenic differentiation process and may ultimately impact bone formation in periodontitis. Mechanistically, it was elucidated that Lockd interacts with SUZ12, a core component of the polycomb repressive complex 2 (PRC2), and may affect the PRC2 complex's role in osteogenic gene expression.ConclusionsLockd boosts the proliferation of M‐MSCs but inhibits their osteogenic differentiation by interacting with SUZ12, potentially inhibiting osteogenic capability in the inflammatory microenvironment.

中文翻译：

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Lockd 通过与炎症微环境中的 SUZ12 结合来增强下颌间充质干细胞增殖，同时抑制成骨能力


目的探讨 lncRNA Lockd 在下颌间充质干细胞 （M-MSC） 增殖和炎症微环境中成骨能力中的作用，重点关注其与 SUZ12 的相互作用。材料和方法使用 lncR Lockd 敲低/过表达细胞模型和小鼠牙周炎模型，我们探讨了 Lockd 对炎症微环境中 M-MSC 增殖和成骨能力的影响。来自多个数据库的预测和一系列拯救实验揭示了 M-MSC 的 Lockd/SUZ12 信号轴在炎症微环境中的调节作用。结果发现 Lockd 刺激 M-MSC 增殖但损害成骨分化。体外研究表明，Lockd 的激活对成骨分化过程产生负性抑制，并可能最终影响牙周炎的骨形成。从机制上讲，阐明 Lockd 与多梳抑制复合物 2 （PRC2） 的核心成分 SUZ12 相互作用，并可能影响 PRC2 复合物在成骨基因表达中的作用。结论Lockd 促进 M-MSCs 的增殖，但通过与 SUZ12 相互作用抑制其成骨分化，可能抑制炎症微环境中的成骨能力。