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A vitronectin-derived peptide prevents and restores alveolar bone loss by modulating bone re-modelling and expression of RANKL and IL-17A
DC Field | Value | Language |
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dc.contributor.author | Lee, Junbeom | - |
dc.contributor.author | Min, Hong Ki | - |
dc.contributor.author | Park, Cho Yeon | - |
dc.contributor.author | Kang, Hyun Ki | - |
dc.contributor.author | Jung, Sung Youn | - |
dc.contributor.author | Min, Byung-Moo | - |
dc.date.accessioned | 2022-10-05T04:15:33Z | - |
dc.date.available | 2022-10-05T04:15:33Z | - |
dc.date.created | 2022-08-17 | - |
dc.date.issued | 2022-08 | - |
dc.identifier.citation | Journal of Clinical Periodontology, Vol.49 No.8, pp.799-813 | - |
dc.identifier.issn | 0303-6979 | - |
dc.identifier.uri | https://hdl.handle.net/10371/185403 | - |
dc.description.abstract | Aim This study investigated whether a vitronectin-derived peptide (VnP-16) prevents and/or reverses alveolar bone resorption induced by ligature-induced periodontitis in rodents and identified the underlying mechanism. Materials and Methods We evaluated the effects of VnP-16 on osteogenic differentiation in human periodontal ligament cells (hPDLCs), lipopolysaccharide-induced inflammatory responses in gingival fibroblasts, and immune response in T lymphocytes. Ligature-induced periodontitis was induced by ligating the bilateral mandibular first molars for 14 days in rats and for 7 days in mice (n = 10/group). VnP-16 (100 mu g/10 mu l) was applied topically into the gingival sulcus of rats via intra-sulcular injection, whereas the peptide (50 mu g/5 mu l) was administered directly into the gingiva of mice via intra-gingival injection. To evaluate the preventive and therapeutic effects of VnP-16, micro-computed tomography analysis and histological staining were then performed. Results VnP-16 promoted osteogenic differentiation of periodontal ligament cells and inhibited the production of lipopolysaccharide-induced inflammatory mediators in gingival fibroblasts. Concomitantly, VnP-16 modulated the host immune response by reducing the number of receptor activator of NF-kappa B ligand (RANKL)-expressing lipopolysaccharide-stimulated CD4(+) and CD8(+) T cells, and by suppressing RANKL and interleukin (IL)-17A production. Furthermore, local administration of VnP-16 in rats and mice significantly prevented and reversed alveolar bone loss induced by ligature-induced periodontitis. VnP-16 enhanced osteoblastogenesis and simultaneously inhibited osteoclastogenesis and suppressed RANKL and IL-17A expression in vivo. Conclusions Our findings suggest that VnP-16 acts as a potent therapeutic agent for preventing and treating periodontitis by regulating bone re-modelling and immune and inflammatory responses. | - |
dc.language | 영어 | - |
dc.publisher | Blackwell Publishing Inc. | - |
dc.title | A vitronectin-derived peptide prevents and restores alveolar bone loss by modulating bone re-modelling and expression of RANKL and IL-17A | - |
dc.type | Article | - |
dc.identifier.doi | 10.1111/jcpe.13671 | - |
dc.citation.journaltitle | Journal of Clinical Periodontology | - |
dc.identifier.wosid | 000811643500001 | - |
dc.identifier.scopusid | 2-s2.0-85131943528 | - |
dc.citation.endpage | 813 | - |
dc.citation.number | 8 | - |
dc.citation.startpage | 799 | - |
dc.citation.volume | 49 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Min, Hong Ki | - |
dc.contributor.affiliatedAuthor | Min, Byung-Moo | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
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