PDF(Pubmed)
Abstract：
MicroRNA-155 (miR-155) is a multifunctional miRNA whose expression is known to be involved in a range of physiological and pathological processes. Its association with several oral diseases has been established. However, the specific role of miR-155 in orthodontic tooth movement remains unclear. In this study, we investigated the impact of miR-155 on osteoclast differentiation and orthodontic tooth movement models, aiming to explore the underlying mechanisms.
In this experiment, we utilized various agents including miR-155 mimic, miR-155 inhibitor, as well as non-specific sequences (NC mimic & NC inhibitor) to treat murine BMMNCs. Subsequently, osteoclast induction (OC) was carried out to examine the changes in the differentiation ability of monocytes under different conditions. To assess these changes, we employed RT-PCR, Western blotting, and TRAP staining techniques. For the orthodontic tooth movement model in mice, the subjects were divided into two groups: the NaCl group (injected with saline solution) and the miR-155 inhibitor group (injected with AntagomiR-155). We observed the impact of orthodontic tooth movement using stereoscopic microscopy, micro-CT, and HE staining. Furthermore, we performed RT-PCR and Western blotting analyses on the tissues surrounding the moving teeth. Additionally, we employed TargetScan to predict potential target genes of miR-155.
During osteoclast induction of BMMNCs, the expression of miR-155 exhibited an inverse correlation with osteoclast-related markers. Overexpression of miR-155 led to a decrease in osteoclast-related indexes, whereas underexpression of miR-155 increased those indexes. In the mouse orthodontic tooth movement model, the rate of tooth movement was enhanced following injection of the miR-155 inhibitor, leading to heightened osteoclast activity. TargetScan analysis identified SOCS1 as a target gene of miR-155.
Our results suggest that miR-155 functions as an inhibitor of osteoclast differentiation, and it appears to regulate osteoclasts during orthodontic tooth movement. The regulatory mechanism of miR-155 in this process involves the targeting of SOCS1.
In this experiment, we utilized various agents including miR-155 mimic, miR-155 inhibitor, as well as non-specific sequences (NC mimic & NC inhibitor) to treat murine BMMNCs. Subsequently, osteoclast induction (OC) was carried out to examine the changes in the differentiation ability of monocytes under different conditions. To assess these changes, we employed RT-PCR, Western blotting, and TRAP staining techniques. For the orthodontic tooth movement model in mice, the subjects were divided into two groups: the NaCl group (injected with saline solution) and the miR-155 inhibitor group (injected with AntagomiR-155). We observed the impact of orthodontic tooth movement using stereoscopic microscopy, micro-CT, and HE staining. Furthermore, we performed RT-PCR and Western blotting analyses on the tissues surrounding the moving teeth. Additionally, we employed TargetScan to predict potential target genes of miR-155.
During osteoclast induction of BMMNCs, the expression of miR-155 exhibited an inverse correlation with osteoclast-related markers. Overexpression of miR-155 led to a decrease in osteoclast-related indexes, whereas underexpression of miR-155 increased those indexes. In the mouse orthodontic tooth movement model, the rate of tooth movement was enhanced following injection of the miR-155 inhibitor, leading to heightened osteoclast activity. TargetScan analysis identified SOCS1 as a target gene of miR-155.
Our results suggest that miR-155 functions as an inhibitor of osteoclast differentiation, and it appears to regulate osteoclasts during orthodontic tooth movement. The regulatory mechanism of miR-155 in this process involves the targeting of SOCS1.
摘要：
背景：MicroRNA-155（miR-155）是一种多功能miRNA，已知其表达涉及一系列生理和病理过程。已确定其与几种口腔疾病的关联。然而,miR-155在正畸牙齿移动中的具体作用尚不清楚.在这项研究中,我们研究了miR-155对破骨细胞分化和正畸牙齿移动模型的影响，旨在探索潜在的机制。
方法：在本实验中，我们利用了各种药物，包括miR-155模拟物，miR-155抑制剂，以及治疗鼠BMMNC的非特异性序列(NC模拟物和NC抑制剂)。随后，进行破骨细胞诱导（OC）以检查单核细胞在不同条件下分化能力的变化。为了评估这些变化，我们采用了RT-PCR,西方印迹,和TRAP染色技术。对于小鼠正畸牙齿移动模型，受试者分为两组:NaCl组(注射生理盐水)和miR-155抑制剂组(注射AntagomiR-155).我们使用立体显微镜观察正畸牙齿移动的影响，Micro-CT,HE染色。此外，我们对移动牙齿周围的组织进行了RT-PCR和Western印迹分析.此外,我们使用TargetScan预测miR-155的潜在靶基因。
结果：在BMMNCs的破骨细胞诱导过程中，miR-155的表达与破骨细胞相关标志物呈负相关.miR-155过表达导致破骨细胞相关指标降低,而miR-155的低表达增加了这些指标。在小鼠正畸牙齿移动模型中,在注射miR-155抑制剂后，牙齿移动速率增强，导致破骨细胞活性增强。TargetScan分析将SOCS1鉴定为miR-155的靶基因。
结论：我们的结果表明miR-155作为破骨细胞分化的抑制剂，它似乎在正畸牙齿移动过程中调节破骨细胞。miR-155在此过程中的调控机制涉及SOCS1的靶向。
方法：在本实验中，我们利用了各种药物，包括miR-155模拟物，miR-155抑制剂，以及治疗鼠BMMNC的非特异性序列(NC模拟物和NC抑制剂)。随后，进行破骨细胞诱导（OC）以检查单核细胞在不同条件下分化能力的变化。为了评估这些变化，我们采用了RT-PCR,西方印迹,和TRAP染色技术。对于小鼠正畸牙齿移动模型，受试者分为两组:NaCl组(注射生理盐水)和miR-155抑制剂组(注射AntagomiR-155).我们使用立体显微镜观察正畸牙齿移动的影响，Micro-CT,HE染色。此外，我们对移动牙齿周围的组织进行了RT-PCR和Western印迹分析.此外,我们使用TargetScan预测miR-155的潜在靶基因。
结果：在BMMNCs的破骨细胞诱导过程中，miR-155的表达与破骨细胞相关标志物呈负相关.miR-155过表达导致破骨细胞相关指标降低,而miR-155的低表达增加了这些指标。在小鼠正畸牙齿移动模型中,在注射miR-155抑制剂后，牙齿移动速率增强，导致破骨细胞活性增强。TargetScan分析将SOCS1鉴定为miR-155的靶基因。
结论：我们的结果表明miR-155作为破骨细胞分化的抑制剂，它似乎在正畸牙齿移动过程中调节破骨细胞。miR-155在此过程中的调控机制涉及SOCS1的靶向。
