Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.
Clinical Research Center of Shaanxi Province for Dental and Maxillofacial Diseases, Department of Endodontics, College of Stomatology, Xi'an Jiaotong University, Xi'an, China.
Int J Med Sci. 2023 May 21;20(7):958-968. doi: 10.7150/ijms.82454. eCollection 2023.
The treatment of bone loss due to periodontitis has posed a great challenge for physicians for decades. Therefore, it is of extraordinary significance to identify an effective regeneration scheme for alveolar bone. This study aimed to investigate long non-coding RNA (lncRNA) small nucleolar RNA host gene 5 (SNHG5) whether sponges microRNA-23b-3p (miR-23b-3p) to achieve the osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs). Results revealed that the expression of SNHG5 was upregulated whereas that of miR-23b-3p was downregulated in osteogenic hPDLSCs. Alizarin red staining assays and qRT-PCR demonstrated that SNHG5 silencing or miR-23b-3p overexpression inhibits hPDLSCs osteogenic differentiation and vice versa. In addition, miR-23b-3p partially abolished the promotive effect of SNHG5 on osteogenic differentiation of hPDLSCs. Dual luciferase report and RNA pulldown assay verified that miR-23b-3p is a regulatory target of SNHG5 and that is a gene target of miR-23b-3p. In brief, the results demonstrate that SNHG5 promotes the osteogenic differentiation of hPDLSCs by regulating the miR-23b-3p/Runx2 axis. Our study provides novel mechanistic insights into the critical role of lncRNA SNHG5 as a miR-23b-3p sponge to regulate Runx2 expression in hPDLSCs and may serve as a potential therapeutics target for periodontitis.
数十年来，治疗牙周炎导致的骨丢失一直是医生面临的巨大挑战。因此，寻找一种有效的牙槽骨再生方案具有重要意义。本研究旨在探讨长链非编码 RNA（lncRNA）小核仁 RNA 宿主基因 5（SNHG5）是否通过海绵 microRNA-23b-3p（miR-23b-3p）来实现人牙周膜干细胞（hPDLSCs）的成骨分化。结果表明，成骨 hPDLSCs 中 SNHG5 的表达上调，而 miR-23b-3p 的表达下调。茜素红染色和 qRT-PCR 结果表明，SNHG5 沉默或 miR-23b-3p 过表达抑制 hPDLSCs 的成骨分化，反之亦然。此外，miR-23b-3p 部分消除了 SNHG5 对 hPDLSCs 成骨分化的促进作用。双荧光素酶报告和 RNA 下拉实验验证了 miR-23b-3p 是 SNHG5 的调节靶点，而 是 miR-23b-3p 的靶基因。总之，这些结果表明，SNHG5 通过调节 miR-23b-3p/Runx2 轴促进 hPDLSCs 的成骨分化。我们的研究为 lncRNA SNHG5 通过作为 miR-23b-3p 的海绵来调节 hPDLSCs 中 Runx2 表达的关键作用提供了新的机制见解，并可能成为牙周炎的潜在治疗靶点。
