Zhengquan He, Yugui Du, Chuhan Peng, Bowen Xu, Jiayue Tang, Runxuan Liu, Kai Yang
{"title":"在大鼠上颌骨扩张模型中,Piezo1 通过 CaMKII 信号促进骨生成","authors":"Zhengquan He, Yugui Du, Chuhan Peng, Bowen Xu, Jiayue Tang, Runxuan Liu, Kai Yang","doi":"10.1111/ocr.12862","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>Rapid maxillary expansion (RME) is a widely used technique to treat maxillary transverse deficiency. Piezo1 is a cation channel that is activated by mechanical force and regulates bone formation. This study aims to elucidate the role of Piezo1 in bone remodelling during the RME process.</p><p><strong>Materials and methods: </strong>In this study, the periosteal-derived stem cells (PDSCs) were cultured and stretched by the Flexcell system. The effects of Piezo1 on osteogenesis were assessed via RNA sequencing, real-time quantitative PCR, and western blot analyses. Moreover, for in vivo analyses, the rat RME model was established. The function of Piezo1 in mid-palatal suture bone remodelling was evaluated using micro-CT, haematoxylin-eosin (HE) staining, and immunohistochemistry analyses.</p><p><strong>Results: </strong>It was revealed that under tension force, the osteogenic factors (Runt-related transcription factor 2, Osterix, and Alkaline Phosphatase) and Ca<sup>2+</sup>/calmodulin -dependent protein kinase (CaMKII) were significantly enhanced in PDSCs over time. Furthermore, these were also upregulated in the RME model with the expansion of the mid-palatal suture. However, Piezo1 inhibition by Grammostola spatulata mechanotoxin 4 downregulated the levels of these factors in the RME model.</p><p><strong>Conclusions: </strong>This study indicated that Piezo1 is associated with the osteogenesis of PDSCs and bone remodelling in the RME process. CaMKII might also participate in this process.</p>","PeriodicalId":19652,"journal":{"name":"Orthodontics & Craniofacial Research","volume":" ","pages":"196-206"},"PeriodicalIF":2.4000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Piezo1 Promotes Osteogenesis Through CaMKII Signalling in a Rat Maxillary Expansion Model.\",\"authors\":\"Zhengquan He, Yugui Du, Chuhan Peng, Bowen Xu, Jiayue Tang, Runxuan Liu, Kai Yang\",\"doi\":\"10.1111/ocr.12862\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objectives: </strong>Rapid maxillary expansion (RME) is a widely used technique to treat maxillary transverse deficiency. Piezo1 is a cation channel that is activated by mechanical force and regulates bone formation. This study aims to elucidate the role of Piezo1 in bone remodelling during the RME process.</p><p><strong>Materials and methods: </strong>In this study, the periosteal-derived stem cells (PDSCs) were cultured and stretched by the Flexcell system. The effects of Piezo1 on osteogenesis were assessed via RNA sequencing, real-time quantitative PCR, and western blot analyses. Moreover, for in vivo analyses, the rat RME model was established. The function of Piezo1 in mid-palatal suture bone remodelling was evaluated using micro-CT, haematoxylin-eosin (HE) staining, and immunohistochemistry analyses.</p><p><strong>Results: </strong>It was revealed that under tension force, the osteogenic factors (Runt-related transcription factor 2, Osterix, and Alkaline Phosphatase) and Ca<sup>2+</sup>/calmodulin -dependent protein kinase (CaMKII) were significantly enhanced in PDSCs over time. Furthermore, these were also upregulated in the RME model with the expansion of the mid-palatal suture. However, Piezo1 inhibition by Grammostola spatulata mechanotoxin 4 downregulated the levels of these factors in the RME model.</p><p><strong>Conclusions: </strong>This study indicated that Piezo1 is associated with the osteogenesis of PDSCs and bone remodelling in the RME process. 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Piezo1 Promotes Osteogenesis Through CaMKII Signalling in a Rat Maxillary Expansion Model.
Objectives: Rapid maxillary expansion (RME) is a widely used technique to treat maxillary transverse deficiency. Piezo1 is a cation channel that is activated by mechanical force and regulates bone formation. This study aims to elucidate the role of Piezo1 in bone remodelling during the RME process.
Materials and methods: In this study, the periosteal-derived stem cells (PDSCs) were cultured and stretched by the Flexcell system. The effects of Piezo1 on osteogenesis were assessed via RNA sequencing, real-time quantitative PCR, and western blot analyses. Moreover, for in vivo analyses, the rat RME model was established. The function of Piezo1 in mid-palatal suture bone remodelling was evaluated using micro-CT, haematoxylin-eosin (HE) staining, and immunohistochemistry analyses.
Results: It was revealed that under tension force, the osteogenic factors (Runt-related transcription factor 2, Osterix, and Alkaline Phosphatase) and Ca2+/calmodulin -dependent protein kinase (CaMKII) were significantly enhanced in PDSCs over time. Furthermore, these were also upregulated in the RME model with the expansion of the mid-palatal suture. However, Piezo1 inhibition by Grammostola spatulata mechanotoxin 4 downregulated the levels of these factors in the RME model.
Conclusions: This study indicated that Piezo1 is associated with the osteogenesis of PDSCs and bone remodelling in the RME process. CaMKII might also participate in this process.
期刊介绍:
Orthodontics & Craniofacial Research - Genes, Growth and Development is published to serve its readers as an international forum for the presentation and critical discussion of issues pertinent to the advancement of the specialty of orthodontics and the evidence-based knowledge of craniofacial growth and development. This forum is based on scientifically supported information, but also includes minority and conflicting opinions.
The objective of the journal is to facilitate effective communication between the research community and practicing clinicians. Original papers of high scientific quality that report the findings of clinical trials, clinical epidemiology, and novel therapeutic or diagnostic approaches are appropriate submissions. Similarly, we welcome papers in genetics, developmental biology, syndromology, surgery, speech and hearing, and other biomedical disciplines related to clinical orthodontics and normal and abnormal craniofacial growth and development. In addition to original and basic research, the journal publishes concise reviews, case reports of substantial value, invited essays, letters, and announcements.
The journal is published quarterly. The review of submitted papers will be coordinated by the editor and members of the editorial board. It is policy to review manuscripts within 3 to 4 weeks of receipt and to publish within 3 to 6 months of acceptance.