For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
10
views
41
references
 Top references
cited by
6
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      380
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Long non-coding RNA SNHG5 promotes the osteogenic differentiation of bone marrow mesenchymal stem cells via the miR-212-3p/GDF5/SMAD pathway

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          The treatment of bone loss has posed a challenge to clinicians for decades. Thus, it is of great significance to identify more effective methods for bone regeneration. However, the role and mechanisms of long non-coding RNA small nucleolar RNA host gene 5 (SNHG5) during osteogenic differentiation remain unclear.

          Methods

          We investigated the function of SNHG5, Yin Yang 1 (YY1), miR-212-3p and growth differentiation factor 5 (GDF5) in osteogenic differentiation of human bone marrow mesenchymal stem cells (hBMSCs) in vitro and in vivo. Molecular mechanisms were clarified by chromatin immunoprecipitation assay and dual luciferase reporter assay.

          Results

          We found SNHG5 expression was upregulated during osteogenesis of hBMSCs. Knockdown of SNHG5 in hBMSCs inhibited osteogenic differentiation while overexpression of SNHG5 promoted osteogenesis. Moreover, YY1 transcription factor directly bound to the promoter region of SNHG5 and regulated SNHG5 expression to promote osteogenesis. Dual luciferase reporter assay confirmed that SNHG5 acted as a miR-212-3p sponge and miR-212-3p directly targeted GDF5 and further activated Smad1/5/8 phosphorylation. miR-212-3p inhibited osteogenic differentiation, while GDF5 promoted osteogenic differentiation of hBMSCs. In addition, calvarial defect experiments showed knockdown of SNHG5 and GDF5 inhibited new bone formation in vivo.

          Conclusion

          Our results demonstrated that the novel pathway YY1/SNHG5/miR-212-3p/GDF5/Smad regulates osteogenic differentiation of hBMSCs and may serve as a potential target for the treatment of bone loss.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s13287-022-02781-8.

          Related collections

          Most cited references41

          • Record: found
          • Abstract: found
          • Article: not found

          A ceRNA hypothesis: the Rosetta Stone of a hidden RNA language?

          Leonardo Salmena, Laura Poliseno, Yvonne Tay … (2011)
          Here, we present a unifying hypothesis about how messenger RNAs, transcribed pseudogenes, and long noncoding RNAs "talk" to each other using microRNA response elements (MREs) as letters of a new language. We propose that this "competing endogenous RNA" (ceRNA) activity forms a large-scale regulatory network across the transcriptome, greatly expanding the functional genetic information in the human genome and playing important roles in pathological conditions, such as cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
          Article 0 comments Cited 1949 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Mechanisms of TGF-beta signaling from cell membrane to the nucleus.

            Yigong Shi, Joan Massagué (2003)
            TGF-beta signaling controls a plethora of cellular responses and figures prominently in animal development. Recent cellular, biochemical, and structural studies have revealed significant insight into the mechanisms of the activation of TGF-beta receptors through ligand binding, the activation of Smad proteins through phosphorylation, the transcriptional regulation of target gene expression, and the control of Smad protein activity and degradation. This article reviews these latest advances and presents our current understanding on the mechanisms of TGF-beta signaling from cell membrane to the nucleus.
            Article 0 comments Cited 235 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Desperately seeking microRNA targets.

              Marshall Thomas, Judy Lieberman, Ashish Lal (2010)
              MicroRNAs (miRNAs) suppress gene expression by inhibiting translation, promoting mRNA decay or both. Each miRNA may regulate hundreds of genes to control the cell's response to developmental and other environmental cues. The best way to understand the function of a miRNA is to identify the genes that it regulates. Target gene identification is challenging because miRNAs bind to their target mRNAs by partial complementarity over a short sequence, suppression of an individual target gene is often small, and the rules of targeting are not completely understood. Here we review computational and experimental approaches to the identification of miRNA-regulated genes. The examination of changes in gene expression that occur when miRNA expression is altered and biochemical isolation of miRNA-associated transcripts complement target prediction algorithms. Bioinformatic analysis of over-represented pathways and nodes in protein-DNA interactomes formed from experimental candidate miRNA gene target lists can focus attention on biologically significant target genes.
              Article 0 comments Cited 180 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Yunfei Zheng: yunfei_zheng@bjmu.edu.cn
                Weiran Li:
                ORCID: http://orcid.org/0000-0001-9895-1143
                weiranli@bjmu.edu.cn
                Journal
                Journal ID (nlm-ta): Stem Cell Res Ther
                Journal ID (iso-abbrev): Stem Cell Res Ther
                Title: Stem Cell Research & Therapy
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1757-6512
                Publication date (Electronic): 28 March 2022
                Publication date PMC-release: 28 March 2022
                Publication date Collection: 2022
                Volume: 13
                Electronic Location Identifier: 130
                Affiliations
                [1 ]GRID grid.11135.37, ISNI 0000 0001 2256 9319, Department of Orthodontics, , Peking University School and Hospital of Stomatology, ; 22 Zhongguancun Avenue South, Haidian District, Beijing, 100081 People’s Republic of China
                [2 ]GRID grid.11135.37, ISNI 0000 0001 2256 9319, Department of Oral and Maxillofacial Surgery, , Peking University School and Hospital of Stomatology, ; 22 Zhongguancun Avenue South, Haidian District, Beijing, 100081 People’s Republic of China
                [3 ]GRID grid.11135.37, ISNI 0000 0001 2256 9319, Central Laboratory, , Peking University School and Hospital of Stomatology, ; 22 Zhongguancun Avenue South, Haidian District, Beijing, 100081 People’s Republic of China
                Author information
                http://orcid.org/0000-0001-9895-1143
                Article
                Publisher ID: 2781
                DOI: 10.1186/s13287-022-02781-8
                PMC ID: 8962127
                PubMed ID: 35346361
                SO-VID: 55bf5b9e-58c0-4a91-b7fe-9488c5c82932
                Copyright © © The Author(s) 2022
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 29 June 2021
                Date accepted : 23 August 2021
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, national natural science foundation of china;
                Award ID: 82071142
                Award ID: 82071119
                Award Recipient :
                Categories
                Subject: Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2022

                ScienceOpen disciplines: Molecular medicine
                Keywords: snhg5,osteogenesis,yy1,mir-212-3p,gdf5
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: snhg5, osteogenesis, yy1, mir-212-3p, gdf5

                Comments

                Comment on this article

                scite_

                Similar content380

                See all similar

                Cited by5

                See all cited by

                Most referenced authors571

                See all reference authors