ArticleCell proliferation2022
Activation of the pattern recognition receptor NOD1 in periodontitis impairs the osteogenic capacity of human periodontal ligament stem cells via p38/MAPK signalling.
Article in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Phytochemicals in Treatment of Periodontal Disease: A Review of Mechanisms and Roles.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- GelMA@ginsenoside Rb3 Targets Inflammatory Microenvironment in Periodontitis via MAPK Pathway.Gels (Basel, Switzerland) · 2025Article
- Thiostrepton: multifaceted biological activities and its applications in treatment of inflammatory diseases.Inflammopharmacology · 2025Review
- Review
- GroEL triggers NLRP3 inflammasome activation through the TLR/NF-κB p-p65 axis in human periodontal ligament stem cells.Acta biochimica et biophysica Sinica · 2024Article
- [Research Progress of Cellular Lipid Droplets in Oral Diseases].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024Review
- AFF4 regulates osteogenic potential of human periodontal ligament stem cells via mTOR-ULK1-autophagy axis.Cell proliferation · 2024Article
- Osteocyte RANKL Drives Bone Resorption in Mouse Ligature-Induced Periodontitis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Activation of the pattern recognition receptor NOD1 in periodontitis impairs the osteogenic capacity of human periodontal ligament stem cells via p38/MAPK signalling.Cell proliferation · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectivesNucleotide oligomerization domain receptor 1 (NOD1) mediates host recognition of pathogenic bacteria in periodontium. However, the specific role of NOD1 in regulating osteogenesis is unclear. Therefore, this study focused on the activation status of NOD1 in periodontitis and its effect on the osteogenic capacity of human periodontal ligament stem cells (hPDLSCs) as well as the underlying mechanism.
methodsHistological staining and Western blot were utilized to assess NOD1 expression in the periodontium of people with or without periodontitis. HPDLSCs were cultured under NOD1 agonist or antagonist treatment. Q-PCR and Western blot were employed to assess the expression of osteogenic marker genes and proteins. Alizarin red staining and alkaline phosphatase staining were used to determine the osteogenic capability of hPDLSCs. The activation of downstream signalling was determined and specific inhibitors were utilized to confirm the signalling pathway in NOD1-regulated osteogenesis.
resultsNOD1 expression is significantly elevated in periodontitis. With NOD1 activated by particular agonist tri-DAP, the osteogenic potential of hPDLSCs was impaired. NOD1 antagonist co-incubation partially restored the decreased osteogenesis in hPDLSCs. P38/MAPK was phosphorylated in tri-DAP-induced NOD1 activation. The inhibitor of p38 rescued the suppression of osteogenesis induced by tri-DAP in hPDLSCs.
conclusionsOur study revealed the expression status of NOD1 in periodontitis. Its activation greatly decreased the osteogenic capacity of hPDLSCs which was mediated by the phosphorylation of p38 downstream signalling.
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