ArticleCellular and molecular life sciences : CMLS2024
NOR1 promotes the osteoblastic differentiation of human periodontal ligament stem cells via TGF-β signaling pathway.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Transcutaneous auricular vagus nerve stimulation attenuates depressive-like behaviors via enhancing neuroplasticity and regulating the ALK5/Smad2/3/Gadd45β signaling pathway in rats with post-stroke depression.Frontiers in immunology · 2026Article
- Photobiomodulation-pretreated dental follicle stem cells with enhanced osteogenic function improve alveolar bone regeneration.BMC oral health · 2025Article
- Decoding Dental Stem Cell Aging: Mechanisms, Therapeutic Strategies, and Beyond.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Ferroptosis in periodontitis: mechanisms, impacts, and systemic connections.Cell death discovery · 2025Review
- GDF15 promotes osteogenic differentiation of human dental pulp stem cells by activating the TGF-β/SMAD signaling pathway.Journal of tissue engineeringArticle
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Authors and funding
9 authors.
Funding
Abstract
Alveolar bone loss is a main manifestation of periodontitis. Human periodontal ligament stem cells (PDLSCs) are considered as optimal seed cells for alveolar bone regeneration due to its mesenchymal stem cell like properties. Osteogenic potential is the premise for PDLSCs to repair alveolar bone loss. However, the mechanism regulating osteogenic differentiation of PDLSCs remain elusive. In this study, we identified Neuron-derived orphan receptor 1 (NOR1), was particularly expressed in PDL tissue in vivo and gradually increased during osteogenic differentiation of PDLSCs in vitro. Knockdown of NOR1 in hPDLSCs inhibited their osteogenic potential while NOR1 overexpression reversed this effect. In order to elucidate the downstream regulatory network of NOR1, RNA-sequencing was used. We found that downregulated genes were mainly enriched in TGF-β, Hippo, Wnt signaling pathway. Further, by western blot analysis, we verified that the expression level of phosphorylated-SMAD2/3 and phosphorylated-SMAD4 were all decreased after NOR1 knockdown. Additionally, ChIP-qPCR and dual luciferase reporter assay indicated that NOR1 could bind to the promoter of TGFBR1 and regulate its activity. Moreover, overexpression of TGFBR1 in PDLSCs could rescue the damaged osteogenic potential after NOR1 knockdown. Taken together, our results demonstrated that NOR1 could activate TGF-β/SMAD signaling pathway and positively regulates the commitment of osteoblast lineages of PDLSCs by targeting TGFBR1 directly.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.