骨膜蛋白基因敲除鼠正畸牙齿移动模型的建立及验证  

Construction and validation of orthodontic tooth movement model in periostin knockout mice

作　　者：郭薇 房付春[2] 徐会勇[2] 欧阳钧[3] GUO Wei;FANG Fuchun;XU Huiyong;OUYANG Jun(Department of Pathology,Affiliated Stomatological Hospital of Southern Medical University,Guangzhou 510515,China;Departmentof Stomatology,Nanfang Hospital,Southern Medical University,Guangzhou 510515,China;Department of Anatomy,School of BasicMedicine,Southern Medical University,Guangzhou 510515,China)

机构地区：[1]南方医科大学口腔医院病理科,广东广州510510 [2]南方医科大学南方医院口腔科,广东广州510515 [3]南方医科大学基础医学院解剖教研室,广东广州510515

出　　处：《中国医学物理学杂志》2019年第10期1233-1238,共6页Chinese Journal of Medical Physics

基　　金：广东省自然科学基金(2015A030310140)

摘　　要：目的:建立小鼠以及骨膜蛋白(PN)基因敲除小鼠正畸牙齿移动模型,并分析相关信号通路。方法:根据实验条件把小鼠分为4组:C57小鼠未加力组和加力组、PN基因敲除小鼠组上颌加力组和未加力组,每组5只,其中加力组加力5d。处死后,显微CT扫描上下颌骨,并采用RT-PCR检测牙周膜中相关基因的表达水平。结果:与C57小鼠相比,PN基因敲除小鼠的牙槽骨出现明显的吸收,牙周膜连续性中断破坏。在C57小鼠中,加力组牙周膜中的PN、粘着斑激酶(FAK)和TGF-β1表达水平显著增强(P<0.05);在基因敲除鼠中,加力组牙周膜中的FAK(P<0.05)和TGF-β1表达水平显著增强(P<0.01);在同样加力的条件下,C57小鼠与PN基因敲除小鼠相比,TGF-β1显著降低(P<0.05),FAK表达水平显著升高(P<0.01)。结论:PN是正畸作用下牙周膜的改建过程一个重要分子环节,发挥着转导调控作用,TGF-β1--PN--FAK信号通路参与调控正畸作用下牙周膜的改建过程。Objective To establish the orthodontic tooth movement model in periostin (PN) knockout mice and analyze the related signaling pathways. Methods According to experimental conditions, the enrolled mice were divided into 4 groups, namely C57 mice groups with and without receiving orthodontic force, PN knockout groups with and without receiving orthodontic force, with 5 mice in each group, and the orthodontic force was last for 5 days. After the mice were killed, the upper and lower jaws were scanned with Micro-CT;and the expression levels of related genes in periodontal ligament were detected with RT-PCR. Results Compared with C57 mice, PN knockout mice had obvious alveolar bone resorption and continuous destruction of periodontal ligament. The comparison between two groups of C57 mice showed that the expression levels of PN, focal adhesion kinase (FAK) and TGF-β1 in the periodontal ligament of mice receiving orthodontic force were significantly increased (P<0.05). The comparison between two groups of PN knockout mice showed that the expression levels of FAK and TGF-β1 in the periodontal ligament of mice receiving orthodontic force were remarkably increased (P<0.01). Under the same force condition, the expression level of TGF-β1 in C57 mice was significantly lower than that in PN knockout mice (P<0.05), while the expression level of FAK in C57 mice was obviously increased (P<0.01). Conclusion PN which is an important molecular link in the process of periodontal ligament remodeling under orthodontic action plays an important role in transduction and regulation. TGF-β1-- PN--FAK signaling pathway is involved in the process of periodontal ligament remodeling under orthodontic action.

关 键 词：骨膜蛋白 小鼠模型 基因敲除 正畸移动 

分 类 号：R318.01[医药卫生—生物医学工程]