Dataset Information

Long non‑coding RNA SNHG5 promotes osteogenic differentiation of human periodontal ligament stem cells via mediating miR‑23b‑3p/Runx2 axis.

ABSTRACT: 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 Runx2 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.

SUBMITTER: Sun X

PROVIDER: S-EPMC10266046 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature

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Long non‑coding RNA SNHG5 promotes osteogenic differentiation of human periodontal ligament stem cells via mediating miR‑23b‑3p/Runx2 axis.

Sun Xuefei X Li Zhidan Z Dong Shaojie S Dong Qianqian Q

International journal of medical sciences 20230521 7

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 ...[more]

PMID: 37324192

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Project description:BackgroundAn increasing number of studies have shown that dysregulated miR-589-3p is associated with multiple diseases. However, the role of miR-589-3p in osteogenic differentiation of periodontal ligament stem cells (PDLSCs) remains unknown. This study aimed to explore the biological function and potential molecular mechanism of miR-589-3p in osteogenic differentiation of PDLSCs.MethodsGSE159508 was downloaded from Gene Expression Omibus (GEO, http://www.ncbi.nlm.nih.gov/geo/ ). Differentially expressed miRNAs between osteogenic induction PDLSCs versus non-induction PDLSCs were obtained by R software. miR-589-3p mimic and miR-589-3p inhibitor and corresponding negative control were obtained and to identify the role of miR-589-3p in osteogenic differentiation of PDLSCs. ALP staining and ARS were used to evaluate ALP activity and mineralization, respectively. The targeted binding relationship between miR-589-3p and ATF1 was predicted and verified by target prediction analysis and dual-luciferase assay. Furthermore, the functional mechanism based on miR-589-3p and ATF1 in osteogenic differentiation of PDLSCs was further investigated through rescue experiments.ResultsAccording to the cut-off criteria with log 2 FC > 1.0 and P < 0.05, 514 differentially expressed miRNAs were identified between osteogenic induction and non-induction PDLSCs, including 309 upregulated miRNAs and 205 downregulated miRNAs. Compared with control PDLSCs, miR-589-3p expression level was notably increased in PDLSCs that underwent osteogenic induction. The overexpression of miR-589-3p promoted the cell viability of PDLSCs, while the low expression of miR-589-3p had the opposite effect. The dual luciferase reporter assay verified that ATF1 was proved to be a direct target of miR-589-3p in PDLSCs. And overexpressed miR-589-3p reduced the expression of ATF1. Overexpression of miR-589-3p enhanced the osteogenic capacity of PDLSCs, as demonstrated by increases in ALP activity, matrix mineralization, and RUNX2, OCN and OSX expression. In addition, the rescue experiments confirmed that overexpressed ATF1 restored the effects of overexpressed miR-589-3p on cell proliferation and osteogenic differentiation of PDLSCs.ConclusionmiR-589-3p could down-regulate the expression of ATF1, thereby promote the proliferation and osteogenic differentiation of PDLSCs. This finding may provide a new therapeutic target for molecular therapy of periodontitis.

Project description:BackgroundPeriodontal ligament stromal cells (PDLSCs) are ideal cell sources for periodontal tissue repair and regeneration, but little is known about what determines their osteogenic capacity. Long non-coding RNAs (lncRNAs) are important regulatory molecules at both transcriptional and post-transcriptional levels. However, their roles in the osteogenic differentiation of PDLSCs are still largely unknown.MethodsThe expression of lncRNA Fer-1-like family member 4 (FER1L4) during the osteogenic differentiation of PDLSCs was detected by quantitative reverse transcription polymerase chain reaction. Overexpression or knockdown of FER1L4 was used to confirm its regulation of osteogenesis in PDLSCs. Alkaline phosphatase and Alizarin red S staining were used to detect mineral deposition. Dual luciferase reporter assays were used to analyze the binding of miR-874-3p to FER1L4 and vascular endothelial growth factor A (VEGFA). Bone regeneration in critical-sized calvarial defects was assessed in nude mice. New bone formation was analyzed by micro-CT, hematoxylin and eosin staining, Masson's trichrome staining, and immunohistochemical analyses.ResultsFER1L4 levels increased gradually during consecutive osteogenic induction of PDLSCs. Overexpression of FER1L4 promoted the osteogenic differentiation of PDLSCs, as revealed by alkaline phosphatase activity, Alizarin red S staining, and the expression of osteogenic markers, whereas FER1L4 knockdown inhibited these processes. Subsequently, we identified a predicted binding site for miR-874-3p on FER1L4 and confirmed a direct interaction between them. Wild-type FER1L4 reporter activity was significantly inhibited by miR-874-3p, whereas mutant FER1L4 reporter was not affected. MiR-874-3p inhibited osteogenic differentiation and reversed the promotion of osteogenesis in PDLSCs by FER1L4. Moreover, miR-874-3p targeted VEGFA, a crucial gene in osteogenic differentiation, whereas FER1L4 upregulated the expression of VEGFA. In vivo, overexpression of FER1L4 led to more bone formation compared to the control group, as demonstrated by micro-CT and the histologic analyses.ConclusionFER1L4 positively regulates the osteogenic differentiation of PDLSCs via miR-874-3p and VEGFA. Our study provides a promising target for enhancing the osteogenic potential of PDLSCs and periodontal regeneration.

Dataset Information

Long non‑coding RNA SNHG5 promotes osteogenic differentiation of human periodontal ligament stem cells via mediating miR‑23b‑3p/Runx2 axis.

Publications

Long non‑coding RNA SNHG5 promotes osteogenic differentiation of human periodontal ligament stem cells via mediating miR‑23b‑3p/Runx2 axis.

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