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Evaluation of a mouse odontoma model and elucidation of the developmental mechanisms of odontoma

小鼠牙瘤模型的评价及牙瘤发育机制的阐明

基本信息

批准号：
15390572
负责人：
NOZAKI Tadashige
金额：
$ 7.1万
依托单位：
Osaka Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2005
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15390572/
关键词：
odontoma differentiation odontoblast ameloblast ghost cell PARP1 遺伝子操作 odontoma Parp-1 ノックアウトマウス

项目摘要

Poly (ADP-ribose) polymerase (Parp1) is known to play roles in cell death and cell differentiation through transcriptional control. In the present study, decalcified mandibles, including the incisors, from Parp1-/- and wild-type Parp1^<+/+> mice with a genetic background of ICR/129Sv maintained on a basal diet for 2 years were subjected to histological analyses. A total of 10 samples from male Parp1^<-/-> mice and 13 samples from male Parp1^<+/+> mice were analyzed. In all samples from the Parp1^<-/-> mice, the dentin showed remarkable proliferation and irregularly lined odontoblasts were observed on the inside of the dental pulp cavity. In contrast, the odontoblasts in the samples from the Parp1^<+/+> mice were regularly lined up on the side of the dental pulp and no abnormalities of the enamel were observed. To elucidate the involvement of PARP1 in the development of human odontoma, samples obtained from 7 complex type and 6 compound type human odontoma cases were analyzed immunohist … More ochemically for their expressions of PARP1. The results revealed that PARP1 was expressed in tooth germ-like tissue, reduced enamel epithelium, immature dentin and immature enamel in the odontomas. Moreover, its expression was detected in odontoblasts and the epithelial component corresponding to ameloblasts. These findings indicate that PARP1 contributes to the differentiation of the cells that constitute odontomas. In addition, PARP1 was expressed in the cytoplasm of ghost cells that did not possess a nucleus. The cytoplasm of these ghost cells was also strongly immunostained by the M30CytoDEATH antibody raised against the cleavage site of cytokeratin 18 produced during the process of apoptosis. Since ghost cells are considered to represent a type of degenerative cells that accumulate hard keratins, and some early apoptosis events seem to have occurred, these observations indicate that PARP1 expression in ghost cells undergoing apoptosis contributed to the formation of these cells in odontomas. Less

已知聚 (ADP-核糖) 聚合酶 (Parp1) 通过转录控制在细胞死亡和细胞分化中发挥作用。在本研究中，对具有 ICR/129Sv 遗传背景且维持基础饮食 2 年的 Parp1-/- 和野生型 Parp1^<+/+> 小鼠的脱钙下颌骨（包括门牙）进行了组织学分析。总共分析了来自雄性Parp1^-/->小鼠的10个样品和来自雄性Parp1^<+/+>小鼠的13个样品。在来自Parp1^-/->小鼠的所有样本中，牙本质均表现出显着的增殖，并且在牙髓腔内部观察到排列不规则的成牙本质细胞。相反，Parp1^+/+小鼠样品中的成牙本质细胞规则地排列在牙髓侧面，并且没有观察到牙釉质异常。为了阐明 PARP1 在人类牙瘤发展中的作用，对从 7 例复杂型和 6 例复合型人类牙瘤病例中获得的样本进行了免疫组织化学分析，以了解 PARP1 的表达。结果显示，PARP1在牙瘤样牙胚组织、减少的牙釉质上皮、未成熟牙本质和未成熟牙釉质中表达。此外，在成牙本质细胞和与成釉细胞相对应的上皮成分中检测到其表达。这些发现表明 PARP1 有助于构成牙瘤的细胞的分化。此外，PARP1在不具有细胞核的鬼细胞的细胞质中表达。这些鬼细胞的细胞质也被 M30CytoDEATH 抗体强烈免疫染色，该抗体针对细胞凋亡过程中产生的细胞角蛋白 18 的裂解位点而产生。由于鬼细胞被认为是一种积累硬角蛋白的退行性细胞，并且似乎已经发生了一些早期凋亡事件，因此这些观察结果表明，正在经历凋亡的鬼细胞中的PARP1表达有助于牙瘤中这些细胞的形成。较少的