ArticleCytotechnology2018
Repeated stimulation by LPS promotes the senescence of DPSCs via TLR4/MyD88-NF-κB-p53/p21 signaling.
Article in Cytotechnology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Role of Lipopolysaccharide, Derived from Various Bacterial Species, in Pulpitis-A Systematic Review.Biomolecules · 2022Pooled it
- Mesenchymal stem/stromal cell senescence in aging and regenerative medicine: a systematic review.Biogerontology · 2026Review
- Inflammation-Regeneration Axis of Dental Pulp Stem Cells: Wnt/NF-κB Crosstalk.International endodontic journal · 2026Review
- Resolvin D1 attenuates senescence-associated secretory phenotype independently of TGF-β-driven cardiac fibroblasts differentiation to myofibroblast.Journal of inflammation (London, England) · 2026Article
- Tooth Decay Promotes Senescence in Dental Pulp Stem Cells, Modifying Their Biological and Proteomic Profiles.Journal of cellular physiology · 2026Article
- Dual effects of 1α,25-dihydroxyvitamin DJournal of dental sciences · 2026Article
- Lipopolysaccharides Modulate Cellular Responses in Dental Pulp Cells.International journal of dentistry · 2026Review
- Exploring the intricate link between gut microbiota dysbiosis and the aging process: implications for age-related diseases.Gut pathogens · 2025Review
- Senescence of dental pulp stem cells: phenotypes, underlying mechanisms and regulatory molecules.Human cell · 2025Review
- Targeting p53-p21 signaling to enhance mesenchymal stem cell regenerative potential.Regenerative therapy · 2025Review
- Activating Transcription Factor 3 (ATF3) Regulates Cellular Senescence and Osteoclastogenesis via STAT3/ERK and p65/AP-1 Pathways in Human Periodontal Ligament Cells.International journal of molecular sciences · 2025Article
- Exendin-4 Reduces Senescence of Inflammation-Induced Periodontal Ligament Stem Cells Through SIRT1/Notch1 Signaling.Stem cells international · 2025Article
- LL-37 regulates odontogenic differentiation of dental pulp stem cells in an inflammatory microenvironment.Stem cell research & therapy · 2024Article
- Cellular senescence: A new perspective on the suppression of periodontitis (Review).Molecular medicine reports · 2024Review
- Article
- Nucleoredoxin Redox Interactions Are Sensitized by Aging and Potentiated by Chronic Alcohol Consumption in the Mouse Liver.Antioxidants (Basel, Switzerland) · 2024Article
- The potential use of ascorbic acid to recover the cellular senescence of lipopolysaccharide-induced human apical papilla cells: an in vitro study.Clinical oral investigations · 2023Article
- Biological Effects of "Inflammageing" on Human Oral Cells: Insights into a Potential Confounder of Age-Related Diseases.International journal of molecular sciences · 2023Article
- Inflammatory response in mouse lungs to haze episodes under different backgrounds of particulate matter exposure.Scientific reports · 2023Article
- Mesenchymal Stromal Cells as a Driver of Inflammaging.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Dental pulp stem cells (DPSCs), one type of mesenchymal stem cells, are considered to be a type of tool cells for regenerative medicine and tissue engineering. Our previous studies found that the stimulation with lipopolysaccharide (LPS) might introduce senescence of DPSCs, and this senescence would have a positive correlation with the concentration of LPS. The β-galactosidase (SA-β-gal) staining was used to evaluate the senescence of DPSCs and immunofluorescence to show the morphology of DPSCs. Our findings suggested that the activity of SA-β-gal has increased after repeated stimulation with LPS and the morphology of DPSCs has changed with the stimulation with LPS. We also found that LPS bound to the Toll-like receptor 4 (TLR4)/myeloid differentiation factor (MyD) 88 signaling pathway. Protein and mRNA expression of TLR4, MyD88 were enhanced in DPSCs with LPS stimulation, resulting in the activation of nuclear factor-κB (NF-κB) signaling, which exhibited the expression of p65 improved in the nucleus while the decreasing of IκB-α. Simultaneously, the expression of p53 and p21, the downstream proteins of the NF-κB signaling, has increased. In summary, DPSCs tend to undergo senescence after repeated stimulation in an inflammatory microenvironment. Ultimately, these findings may lead to a new direction for cell-based therapy in oral diseases and other regenerative medicines.
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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 OpenQuestion graph.