首页> 外文期刊>European journal of oral sciences >Sodium‐chloride‐induced effects on the expression profile of human periodontal ligament fibroblasts with focus on simulated orthodontic tooth movement
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Sodium‐chloride‐induced effects on the expression profile of human periodontal ligament fibroblasts with focus on simulated orthodontic tooth movement

机译:氯化钠诱导对人牙周韧带成纤维细胞表达谱的影响,重点是模拟正畸牙齿运动

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摘要

Increased salt (NaCl) consumption triggers chronic diseases such as hypertension or osteopenia. Its impact on orthodontic tooth movement and periodontitis, however, has not been investigated, although both processes are related to the immune system, with periodontal ligament fibroblasts ( PDLF s) playing a key mediating role. Here, we investigated the impact of NaCl on the expression pattern of PDLF s in a model of simulated compressive orthodontic strain. Periodontal ligament fibroblasts were preincubated for 24?h with additional 0 or 40? mM NaCl and concurrently treated for another 48?h with or without compressive strain of 2?g?cm ?2 . We analyzed the expression of genes and proteins involved in orthodontic tooth movement by reverse transcription?quantitative polymerase chain reaction ( RT ‐ qPCR ), ELISA , and immunoblot. Co‐culture experiments were performed to observe PDLF ‐mediated osteoclastogenesis. A higher (40? mM ) concentration of NaCl in the culture medium resulted in increased secretion of prostaglandin, expression of alkaline phosphatase, and expression of genes involved in extracellular matrix remodeling, but decreased compression‐induced expression of the interleukin‐6 ( IL 6 ) gene. The 40? mM concentration of NaCl also enhanced receptor activator of nuclear factor kappa‐B ligand ( RANKL ) but reduced that of osteoprotegerin ( OPG ), resulting in upregulated PDLF ‐mediated osteoclastogenesis. A high NaCl concentration in the periodontal ligament, corresponding to a high‐salt diet in vivo, may influence orthodontic tooth movement and periodontitis through increased secretion of prostaglandins by PDLF s and upregulated PDLF ‐mediated osteoclastogenesis, possibly accelerating orthodontic tooth movement and propagating periodontitis and periodontal bone loss.
机译:增加的盐(NaCl)消费触发慢性疾病,例如高血压或骨赘。然而,它对正畸牙齿运动和牙周炎的影响尚未研究,尽管这两个过程都与免疫系统有关,但牙周韧带成纤维细胞(PDLF S)发挥着关键的介质作用。在这里,我们研究了NaCl对模拟压缩正畸菌株模型中PDLF S表达模式的影响。用另外的0或40预孵育牙周韧带成纤维细胞24μl? MM NaCl并同时处理另外48ΩHΩ,或者没有压缩菌株2?G?cm≤2。我们通过逆转录分析了基因和蛋白质的表达,通过逆转录Δ定量聚合酶链反应(RT - QPCR),ELISA和免疫印迹。进行共培养实验以观察PDLF介导的骨酸发生。培养基中的NaCl浓度较高(40?mm)导致前列腺素的分泌增加,碱性磷酸酶的表达,以及参与细胞外基质重塑的基因的表达,但是降低了白细胞介素-6的压缩诱导的表达(IL 6基因。 40? MM浓度NaCl也增强了核因子Kappa-B配体(RANKL)的受体激活剂,但降低了骨蛋白酶(OPG)的核心蛋白(OPG),导致上调的PDLF介导的骨质细胞发生。牙周韧带中的高NaCl浓度对应于体内高盐饮食,可以通过PDLF S和上调的PDLF介导的骨酸发生发生,通过增加前列腺素分泌,可能加速正畸牙齿运动和繁殖牙周炎和繁殖牙周炎牙周骨质损失。

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