Small nucleolar RNA host gene 5 plays a role in orthodontic tooth movement by inhibiting osteoclast differentiation

IF 2.4 3区医学 Q2 DENTISTRY, ORAL SURGERY & MEDICINE

Orthodontics & Craniofacial Research Pub Date : 2024-05-07 DOI:10.1111/ocr.12794

Jingjing Feng, Anqi Tan, Weiran Li, Yunfei Zheng

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引用次数: 0

Abstract

Background and Objectives

The alveolar bone remodelling promoted by reasonable mechanical force triggers orthodontic tooth movement (OTM). The generation of osteoclasts is essential in this process. However, the mechanism of mechanical force mediating osteoclast differentiation remains elusive. Small nucleolar RNA host gene 5 (SNHG5), which was reported to mediate the osteogenic differentiation of bone marrow mesenchymal stem cells in our previous study, was downregulated in human periodontal ligament cells (hPDLCs) under mechanical force. At the same time, the RANKL/OPG ratio increased. Based on this, we probed into the role of SNHG5 in osteoclast formation during OTM and the relevant mechanism.

Materials and Methods

SNHG5 and the RANKL/OPG ratio under different compressive forces were detected by western blotting (WB) and qRT-PCR. Impact of overexpression or knockdown of SNHG5 on osteoclast differentiation was detected by qRT-PCR, WB and transwell experiments. The combination of SNHG5 and C/EBPβ was verified by RNA immunoprecipitation and RNA pull-down assays. The expression of SNHG5 and osteoclast markers in gingiva were analysed by qRT-PCR and the paraffin sections of periodontal tissues were used for histological analysis.

Results

Compressive force downregulated SNHG5 and upregulated the RANKL/OPG ratio in hPDLCs. Overexpression of SNHG5 inhibited RANKL's expression and osteoclast differentiation. SNHG5 combined with C/EBPβ, a regulator of osteoclast. The expression of SNHG5 in periodontal tissue decreased during OTM.

Conclusion

SNHG5 inhibited osteoclast differentiation during OTM, achieved by affecting RANKL secretion, which may provide a new idea to interfere with bone resorption during orthodontic treatment.

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小核糖核酸宿主基因 5 通过抑制破骨细胞分化在牙齿矫正过程中发挥作用。

背景和目的：合理的机械力促进的牙槽骨重塑会引发正畸牙齿移动（OTM）。破骨细胞的生成在这一过程中至关重要。然而，机械力介导破骨细胞分化的机制仍不明确。在我们之前的研究中，小核RNA宿主基因5（SNHG5）被报道可介导骨髓间充质干细胞的成骨分化，而在机械力作用下，人牙周韧带细胞（hPDLCs）中的小核RNA宿主基因5被下调。与此同时，RANKL/OPG 比值升高。基于此，我们探究了 SNHG5 在 OTM 过程中破骨细胞形成中的作用及其相关机制：通过Western印迹（WB）和qRT-PCR检测SNHG5和不同压力下的RANKL/OPG比值。通过 qRT-PCR、WB 和 transwell 实验检测过表达或敲除 SNHG5 对破骨细胞分化的影响。通过RNA免疫沉淀和RNA牵引实验验证了SNHG5和C/EBPβ的结合。通过 qRT-PCR 分析 SNHG5 和破骨细胞标记物在牙龈中的表达，并对牙周组织石蜡切片进行组织学分析：结果：压缩力下调了SNHG5，并上调了hPDLCs中RANKL/OPG的比例。过表达 SNHG5 可抑制 RANKL 的表达和破骨细胞的分化。SNHG5 与破骨细胞的调控因子 C/EBPβ 结合。SNHG5在OTM期间在牙周组织中的表达量减少：结论：SNHG5通过影响RANKL的分泌抑制了OTM过程中破骨细胞的分化，这可能为正畸治疗过程中干扰骨吸收提供了一个新思路。

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

Orthodontics & Craniofacial Research 医学-牙科与口腔外科

CiteScore

5.30

自引率

3.20%

发文量

审稿时长

>12 weeks

期刊介绍： Orthodontics & Craniofacial Research - Genes, Growth and Development is published to serve its readers as an international forum for the presentation and critical discussion of issues pertinent to the advancement of the specialty of orthodontics and the evidence-based knowledge of craniofacial growth and development. This forum is based on scientifically supported information, but also includes minority and conflicting opinions. The objective of the journal is to facilitate effective communication between the research community and practicing clinicians. Original papers of high scientific quality that report the findings of clinical trials, clinical epidemiology, and novel therapeutic or diagnostic approaches are appropriate submissions. Similarly, we welcome papers in genetics, developmental biology, syndromology, surgery, speech and hearing, and other biomedical disciplines related to clinical orthodontics and normal and abnormal craniofacial growth and development. In addition to original and basic research, the journal publishes concise reviews, case reports of substantial value, invited essays, letters, and announcements. The journal is published quarterly. The review of submitted papers will be coordinated by the editor and members of the editorial board. It is policy to review manuscripts within 3 to 4 weeks of receipt and to publish within 3 to 6 months of acceptance.