Lockd Enhances Mandibular Mesenchymal Stem Cell Proliferation While Inhibiting Osteogenic Capability via Binding With SUZ12 in the Inflammatory Microenvironment

IF 5.8 1区医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE Journal of Clinical Periodontology Pub Date : 2024-10-14 DOI:10.1111/jcpe.14076

Yahui Lu, Xiaolei Ruan, Gang Xiao, Yueming Dai, Gen Li, Guanhui Cai, Lihe Zheng, Zhaolan Guan, Wen Sun, Hua Wang

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Abstract

Aim

To 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 Methods

Using 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.

Results

Lockd 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.

Conclusions

Lockd boosts the proliferation of M-MSCs but inhibits their osteogenic differentiation by interacting with SUZ12, potentially inhibiting osteogenic capability in the inflammatory microenvironment.

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

目的研究lncRNA Lockd在炎症微环境中下颌骨间充质干细胞（M-MSC）增殖和成骨能力中的作用，重点是其与SUZ12的相互作用。材料与方法利用lncR Lockd敲除/外显细胞模型和小鼠牙周炎模型，我们探讨了Lockd在炎症微环境中对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挽救实验揭示了 Lockd/SUZ12 信号轴在炎症微环境中对 M-MSC 的调控作用。体外研究表明，Lockd 的激活对成骨分化过程有负面抑制作用，并可能最终影响牙周炎的骨形成。从机理上阐明了Lockd与多聚核抑制复合体2（PRC2）的核心成分SUZ12相互作用，并可能影响PRC2复合体在成骨基因表达中的作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Clinical Periodontology 医学-牙科与口腔外科

CiteScore

13.30

自引率

10.40%

发文量

175

审稿时长

3-8 weeks

期刊介绍： Journal of Clinical Periodontology was founded by the British, Dutch, French, German, Scandinavian, and Swiss Societies of Periodontology. The aim of the Journal of Clinical Periodontology is to provide the platform for exchange of scientific and clinical progress in the field of Periodontology and allied disciplines, and to do so at the highest possible level. The Journal also aims to facilitate the application of new scientific knowledge to the daily practice of the concerned disciplines and addresses both practicing clinicians and academics. The Journal is the official publication of the European Federation of Periodontology but wishes to retain its international scope. The Journal publishes original contributions of high scientific merit in the fields of periodontology and implant dentistry. Its scope encompasses the physiology and pathology of the periodontium, the tissue integration of dental implants, the biology and the modulation of periodontal and alveolar bone healing and regeneration, diagnosis, epidemiology, prevention and therapy of periodontal disease, the clinical aspects of tooth replacement with dental implants, and the comprehensive rehabilitation of the periodontal patient. Review articles by experts on new developments in basic and applied periodontal science and associated dental disciplines, advances in periodontal or implant techniques and procedures, and case reports which illustrate important new information are also welcome.