ArticlePloS one2018
Necrostatin-1 promotes ectopic periodontal tissue like structure regeneration in LPS-treated PDLSCs.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Interaction between p-AMPK and RIPK3 reveals a mechanism by which AdipoAI suppresses necroptosis to attenuate periodontitis.Journal of translational medicine · 2026Article
- Periodontal ligament stem cells in tissue remodeling: from mechanical forces to inflammatory signals.Stem cell research & therapy · 2025Review
- Targeting TYROBP to influence the immune microenvironment and osteogenic differentiation of mesenchymal stem cells.Journal of orthopaedic surgery and research · 2025Article
- Immunologic cell deaths: involvement in the pathogenesis and intervention therapy of periodontitis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- ALDH2 alleviates inflammation and facilitates osteogenic differentiation of periodontal ligament stem cells in periodontitis by blocking ferroptosis via activating Nrf2.Functional & integrative genomics · 2024Article
- Necrostatin-1: a promising compound for neurological disorders.Frontiers in cellular neuroscience · 2024Review
- Necroptosis Mediates Muscle Protein Degradation in a Cachexia Model of Weanling Pig with Lipopolysaccharide Challenge.International journal of molecular sciences · 2023Article
- Overview of the main biological mechanisms linked to changes in periodontal ligament stem cells and the inflammatory microenvironment.Journal of Zhejiang University. Science. B · 2023Review
- Signalling pathways in the osteogenic differentiation of periodontal ligament stem cells.Open life sciences · 2023Review
- Cullin3 aggravates the inflammatory response of periodontal ligament stem cells via regulation of SHH signaling and Nrf2.Bioengineered · 2021Article
- PANoptosis: A New Insight Into Oral Infectious Diseases.Frontiers in immunology · 2021Review
- Inhibition of Endoplasmic Reticulum Stress by 4-Phenyl Butyric Acid Presents Therapeutic Effects on Periodontitis: Experimental StudiesStem cells international · 2021Article
- Association of high HIF-1α levels in serous periodontitis with external root resorption by the NFATc1 pathway.Journal of molecular histology · 2020Article
- Salvianolic Acid C Attenuates LPS-Induced Inflammation and Apoptosis in Human Periodontal Ligament Stem Cells via Toll-Like Receptors 4 (TLR4)/Nuclear Factor kappa B (NF-κB) Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necroptosis is a programmed necrosis, regulated by receptor interacting protein kinase 1(RIP1) and receptor interacting protein kinase 3(RIP3), and could be inhibited by necrostatin-1(Nec-1) specifically. This study aims to evaluate the effect of Nec-1 on LPS-treated periodontal ligament stem cells (PDLSCs). In the research, three groups were established: normal cultured PDLSCs, Porphyromonas gingivalis (Pg)-LPS stimulated PDLSCs and Pg-LPS+Nec-1 treated PDLSCs. The expression of RIP1 and RIP3 and osteogenic differentiation of PDLSCs in three groups were analyzed. Then, we constructed cell aggregates (CA) using PDLSCs, then PDLSCs-CA were combined with Bio-Oss in three groups were transplanted subcutaneously in nude mice to assess their potentials of periodontal tissue regeneration. The results showed that RIP1 and RIP3 were fully expressed in Pg-LPS stimulated PDLSCs and the level increased significantly. Nec-1 inhibited RIP1-RIP3 interaction, and further inhibited necroptosis of PDLSCs in inflammatory state. Moreover, Nec-1 pretreatment ameliorates the osteogenic differentiation of LPS-treated PDLSCs and can effectively promote the cementum like structure ectopic regenerative ability of PDLSCs in nude mice. These findings show RIP1/RIP3-mediated necroptosis is an important mechanism of cell death in PDLSCs. Nec-1 has a protective effect in reducing cell death and promotes ectopic periodontal tissue like structure regeneration by inhibiting necroptosis. Nec-1 is a hopeful therapeutic agent which protects cells from necroptosis and ameliorates functional outcome.
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