ArticleBioMed research international2020
S100A9 Increases IL-6 and RANKL Expressions through MAPKs and STAT3 Signaling Pathways in Osteocyte-Like Cells.
Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- S100A9 Induces RANKL Expression in Osteocytes Utilizing IL-6/sIL-6R Combination and gp130 Signaling Pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- High-resolution profiling of osteocyte transcriptomes via single-nucleus RNA sequencing.JBMR plus · 2026Article
- Evaluation of salivary calprotectin as a marker for screening periodontitis using a latex agglutination turbidimetric immunoassay system: a cross-sectional study.BMC oral health · 2026Article
- The S100 protein family in bladder cancer: mechanisms, clinical value, and targeted therapeutic prospects.Frontiers in oncology · 2025Review
- Advance in molecular mechanisms underlying diabetes related to viral hepatitis infection.Frontiers in cellular and infection microbiology · 2025Review
- Exploring the Role of Hormones and Cytokines in Osteoporosis Development.Biomedicines · 2024Review
- S100A8/A9 promotes endometrial fibrosis via regulating RAGE/JAK2/STAT3 signaling pathway.Communications biology · 2024Article
- Osteocytes directly regulate osteolysis via MYD88 signaling in bacterial bone infection.Nature communications · 2022Article
- Crosstalk between bone and other organs.Medical review (2021) · 2022Review
- Effect of add-on hydroxychloroquine therapy on serum proinflammatory cytokine levels in patients with systemic lupus erythematosus.Scientific reports · 2022Article
- Article
- Impact of Chronic Inflammation in Psoriasis on Bone Metabolism.Frontiers in immunology · 2022Review
- Downregulation of S100A9 Reverses Cisplatin-Resistance and Inhibits Proliferation and Migration in Hypopharyngeal Carcinoma.Journal of oncology · 2022Article
- PAMPs and DAMPs as the Bridge Between Periodontitis and Atherosclerosis: The Potential Therapeutic Targets.Frontiers in cell and developmental biology · 2022Review
- S100A8/S100A9 cytokine acts as a transcriptional coactivator during breast cellular transformation.Science advances · 2021Article
- Biosensor and Lab-on-a-chip Biomarker-identifying Technologies for Oral and Periodontal Diseases.Frontiers in pharmacology · 2020Review
- Early proteomic signatures of impaired maxillary bone remodeling under mechanical stress in type 1 diabetes mellitus.Journal of oral biology and craniofacial researchArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCalprotectin is a heterocomplex of S100A8 and S100A9 and is mainly secreted from neutrophils, monocytes, and chondrocytes in inflammatory condition. Calprotectin binds to RAGE and TLR4 and induces the expression of proinflammatory chemokines and cytokines in various cells. Periodontitis is a chronic inflammatory disease that leads to gingival inflammation and alveolar bone resorption. Calprotectin levels in gingival crevicular fluid of periodontitis patients are higher than healthy patients. In the present study, the effects of S100A8 and S100A9 on the expressions of proinflammatory cytokines and bone metabolism-related factors in mouse osteocyte-like cells (MLO-Y4-A2) were investigated.
designMLO-Y4-A2 cells were treated with S100A8 and S100A9, and the expressions of RAGE, TLR4, RANKL, and several inflammatory cytokines were analyzed by PCR and Western blotting or ELISA methods. To investigate the intracellular signaling pathways, phosphorylation of MAPK and STAT3 was determined by Western blotting, and chemical specific inhibitors and siRNAs were used.
resultsExpressions of IL-6 and RANKL were increased by treatment with S100A9 but not S100A8. However, both S100A8 and S100A9 did not change expression of IL-1
conclusionsThese results indicated that S100A9 induces IL-6 and RANKL production via engagement with RAGE and TLR4 signalings in osteocytes and suggested that S100A9 may play important roles in the periodontal alveolar bone destruction.
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Registered trials
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