Anti-inflammatory Annexin A1 in Periodontitis via Formyl Peptide Receptor 2

膜联蛋白A1 牙周纤维 牙槽 牙周炎 骨吸收 医学 下调和上调 炎症 内科学 膜联蛋白 化学 病理 免疫学 牙科 生物化学 流式细胞术 基因
作者
Masahide Takedachi,Masayuki Murata,Kenji Sawada,K. Kawasaki,Kazuyoshi Kawakami,Atsushi Sugimoto,Chiaki Morimoto,Hiromi Sakashita,Yu Usami,Chiharu Fujihara,Tomoaki Iwayama,Shinya Murakami
出处
期刊:Journal of Dental Research [SAGE Publishing]
标识
DOI:10.1177/00220345251322151
摘要

Although annexin A1 (ANXA1) is known to mediate inflammatory responses through N-formyl peptide receptor 2 (FPR2), the role of the ANXA1-FPR2 signaling pathway in periodontal disease remains unclear. This study investigated the contribution of this pathway to the pathophysiology of periodontal disease. Using a ligature-induced mouse model, we performed histologic analyses to examine ANXA1 and FPR2 expression. We observed upregulation of ANXA1 and FPR2 within the gingiva and periodontal ligament. In vitro analysis of human periodontal ligament cells revealed that interleukin 1β (IL-1β)–induced secretion of IL-8 and granulocyte-macrophage colony-stimulating factor was significantly increased in the presence of WRW4, an FPR2 antagonist. Furthermore, IL-1β–mediated upregulation of IL-8 was significantly enhanced in human periodontal ligament cells by silencing ANXA1 and FPR2 expression via small interfering RNAs. The effect of the ANXA1-FPR2 signaling pathway on periodontal tissue destruction was also examined in murine periodontitis under daily administration of WRW4 or an ANXA1 N-terminal mimetic peptide, Ac2-26, with micro–computed tomography and histologic analyses. WRW4 administration significantly intensified alveolar bone resorption, increased the number of osteoclasts on the alveolar bone surface, and dilated blood vessels in the periodontal ligament. Conversely, Ac2-26 administration significantly mitigated alveolar bone resorption. Collectively, these findings suggest a role for the ANXA1-FPR2 signaling pathway in attenuating the pathogenesis of periodontal disease by regulating localized inflammatory responses within periodontal tissues.

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