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GPX4-mediated bone ferroptosis under mechanical stress decreased bone formation via the YAP-TEAD signalling pathway.
Mengjia, Wang; Jun, Ji; Xin, Zhang; Jiahao, Zhang; Jie, Guo.
Afiliación
  • Mengjia W; Department of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Re
  • Jun J; Department of Orthodontics, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Research Institute of Stomatology, Nanjing University, Nanjing, China.
  • Xin Z; Department of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Re
  • Jiahao Z; Department of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Re
  • Jie G; Department of Orthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Re
J Cell Mol Med ; 28(7): e18231, 2024 04.
Article en En | MEDLINE | ID: mdl-38494855
ABSTRACT
Fracture of the alveolar bone resorption is a common complication in orthodontic treatment, which mainly caused by extreme mechanical loading. However, the ferroptosis with orthodontic tooth movement(OTM) relationship has not been thoroughly described. We here analysed whether ferroptosis is involved in OTM-associated alveolar bone loss. Mouse osteoblasts (MC-3T3) and knockdown glutathione peroxidase 4 (GPX4) MC-3T3 were stimulated with compressive force loading and ferrostatin-1 (Fer-1, a ferroptosis inhibitor), and the changes in lipid peroxidation morphology, expression of ferroptosis-related factors and osteogenesis levels were detected. After establishing the rat experimental OTM model, the changes in ferroptosis-related factors and osteogenesis levels were reevaluated in the same manner. Ferroptosis was involved in mechanical stress regulating osteoblast remodelling, and Fer-1 and erastin affected osteoblasts under compression force loading. Fer-1 regulated ferroptosis and autophagy in MC-3T3 and promoted bone proliferation. GPX4-dependent ferroptosis stimulated the YAP (homologous oncoproteins Yes-associated protein) pathway, and GPX4 promoted ferroptosis via the YAP-TEAD (transcriptional enhanced associate domain) signal pathway under mechanical compression force. The in vivo experiment results were consistent with the in vitro experiment results. Ferroptosis transpires during the motion of orthodontic teeth, with compression force side occurring earlier than stretch side within 4 h. GPX4 plays an important role in alveolar bone loss, while Fer-1 can inhibit the compression force-side alveolar bone loss. GPX4's Hippo-YAP pathway is activated by the lack of compression force in the lateral alveolar bone.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Pérdida de Hueso Alveolar / Ferroptosis Límite: Animals Idioma: En Revista: J Cell Mol Med Asunto de la revista: BIOLOGIA MOLECULAR Año: 2024 Tipo del documento: Article Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Pérdida de Hueso Alveolar / Ferroptosis Límite: Animals Idioma: En Revista: J Cell Mol Med Asunto de la revista: BIOLOGIA MOLECULAR Año: 2024 Tipo del documento: Article Pais de publicación: Reino Unido