ArticleOral diseases2021
Inhibition of sphingosine-1-phosphate receptor 2 attenuated ligature-induced periodontitis in mice.
Article in Oral diseases, 2021. 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, 10 citations in OpenAlex.
- Inhibition of CD38 by 78c Enhanced NADInternational journal of molecular sciences · 2026Article
- Experimental Murine Periodontitis Increases Salivary Gland IgA-Producing B Cells Following Oral Dysbiosis.Microbiology and immunology · 2025Article
- Gli1Journal of dental research · 2024Article
- Inhibition of Sphingosine-1-Phosphate Receptor 2 by JTE013 Enhanced Alveolar Bone Regeneration by Promoting Angiogenesis.International journal of molecular sciences · 2023Article
- The function of Sphingosine-1-phosphate receptor 2 (S1PR2) in maintaining intestinal barrier and inducing ulcerative colitis.Bioengineered · 2022Article
- Inhibition of Sphingosine-1-Phosphate Receptor 2 by JTE013 Promoted Osteogenesis by Increasing Vesicle Trafficking, Wnt/CaInternational journal of molecular sciences · 2021Article
- Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease.International journal of molecular sciences · 2021Review
- Inhibition of sphingosine-1-phosphate receptor 2 attenuated ligature-induced periodontitis in mice.Oral diseases · 2021Article
- Targeting S1PRs as a Therapeutic Strategy for Inflammatory Bone Loss Diseases-Beyond Regulating S1P Signaling.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectivesPeriodontitis is an inflammatory bone loss disease initiated by oral bacterial inflammation. Herein, we determined whether inhibition of sphingosine-1-phosphate receptor 2 (S1PR2, a G protein-coupled receptor) by its specific antagonist, JTE013, could alleviate ligature-induced periodontitis in mice. MATERIALS AND
methodsC57BL/6 mice were placed with silk ligatures at the left maxillary second molar to induce experimental periodontitis. Mice were treated with JTE013 or control vehicle (dimethyl sulfoxide, DMSO) oral topically on the ligatures once daily. After 15 days of treatment, RNA was extracted from the lingual mucosal tissues to quantify IL-1β, IL-6, and TNF mRNA levels in the tissues. Alveolar bone loss was determined by micro-computed tomography. Sagittal periodontal tissue sections were cut and stained by hematoxylin and eosin (H&E) for general histology, or stained by tartrate-resistant acid phosphatase (TRAP) for osteoclasts.
resultsTreatment with JTE013 attenuated ligature-induced alveolar bone loss compared with DMSO treatment. Treatment with JTE013 reduced IL-1β, IL-6, and TNF mRNA levels in murine gingival mucosal tissues, inhibited leukocyte infiltration in the periodontal tissues, and decreased the number of osteoclasts in the periodontal tissues compared with controls.
conclusionOral topical administration of JTE013 alleviated periodontal inflammatory bone loss induced by ligature placement in mice.
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