Evaluation of a mouse odontoma model and elucidation of the developmental mechanisms of odontoma
Evaluation of a mouse odontoma model and elucidation of the developmental mechanisms of odontoma
批准号:
15390572
负责人:
NOZAKI Tadashige
金额:
$7.1万
依托单位:
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
项目状态:
已结题
起止时间:
2003 至 2005
中文摘要
多聚ADP核糖聚合酶(Poly(ADP-ribose)polymerase,Parp 1)通过转录调控在细胞死亡和分化中发挥作用。在本研究中,对来自具有ICR/129 Sv遗传背景的Parp 1-/-和野生型Parp 1 ^<+/+>小鼠的脱钙下颌骨(包括门牙)进行组织学分析,所述小鼠维持基础饮食2年。共分析了来自雄性Parp 1 ^<-/->小鼠的10个样品和来自雄性Parp 1 ^<+/+>小鼠的13个样品。在所有来自Parp 1 ^<-/->小鼠的样本中,牙本质显示出显著的增殖,并且在牙髓腔内侧观察到不规则的成牙本质细胞。相比之下,来自Parp 1 ^<+/+>小鼠的样品中的成牙本质细胞在牙髓侧规则地排列,并且没有观察到釉质的异常。为探讨PARP 1在牙瘤发生发展中的作用,对7例复杂型和6例复合型牙瘤进行免疫组化分析, ...更多信息 PARP 1的表达。结果显示,PARP 1在牙胚样组织、减少的釉质上皮、未成熟牙本质和未成熟釉质中均有表达。此外,它的表达被检测到成牙本质细胞和相应的成釉细胞的上皮成分。这些发现表明PARP 1有助于构成牙瘤的细胞的分化。此外,PARP 1在不具有细胞核的鬼细胞的细胞质中表达。这些血影细胞的细胞质也被M30 CytoDEATH抗体强烈免疫染色,该抗体针对细胞角蛋白18在凋亡过程中产生的切割位点。由于鬼细胞被认为是代表一种类型的退行性细胞,积累硬角蛋白,和一些早期的凋亡事件似乎已经发生,这些观察表明,PARP 1的表达在鬼细胞经历凋亡有助于这些细胞的形成在牙肿瘤。少
英文摘要
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
期刊论文(8)
专著(0)
科研奖励(0)
会议论文
登录
查看更多内容
DOI:
10.1016/j.canlet.2005.10.003
发表时间:
2006-09-08
期刊:
CANCER LETTERS
影响因子:
9.7
作者:
[Gunji, Akemi, Uemura, Akiko, Masutani, Mitsuko]
通讯作者:
Masutani, Mitsuko
Expression of PARP1 in odontoma
PARP1在牙瘤中的表达
DOI:
--
发表时间:
2006
期刊:
J.Meikai Univ.Sch. of Dent. 35(1)(in press)
影响因子:
--
作者:
[Nozaki, T., Watanabe, M., Morita, J., Ohura, K., Kusama, K.]
通讯作者:
K.
DOI:
10.1111/j.1349-7006.2003.tb01472.x
发表时间:
2003-06-01
期刊:
CANCER SCIENCE
影响因子:
5.7
作者:
[Nozaki, T, Fujihara, H, Masutani, M]
通讯作者:
Masutani, M
DOI:
10.1016/s1348-8643(05)80014-x
发表时间:
2005-11-01
期刊:
ORAL SCIENCE INTERNATIONAL
影响因子:
0.5
作者:
[Nozaki, Tadashige, Takeyasu, Masaharu, Ohura, Kiyoshi]
通讯作者:
Ohura, Kiyoshi
Study on extra-cellular function mediated by functional RNAs in exosomes secreted from pluripotent stem cells
-
批准号:18K09803
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.83万
-
财政年份:2018
-
负责人:NOZAKI Tadashige
-
依托单位:
Study on characteristics of small RNA secreted from the pluripotent stem cells
-
批准号:15K11283
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.08万
-
财政年份:2015
-
负责人:NOZAKI Tadashige
-
依托单位:
Study on mechanisms for reprogramming factors inducing pluripotency
-
批准号:24593020
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.41万
-
财政年份:2012
-
负责人:NOZAKI Tadashige
-
依托单位:
Studies on the regulation of differentiation of the pluripotent dental pulp stem cells by non-coding RNA
-
批准号:21592547
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$3.0万
-
财政年份:2009
-
负责人:NOZAKI Tadashige
-
依托单位:
Studies on the regenerative medicine utilizing the plasticity of dental pulp stem cells
-
批准号:18592211
-
项目类别:Grant-in-Aid for Scientific Research (C)
-
资助金额:$2.57万
-
财政年份:2006
-
负责人:NOZAKI Tadashige
-
依托单位:
国内基金
海外基金
登录
查看更多内容
Foxc2介导Syap1/Akt信号通路调控破骨/成骨细胞分化促进颞下颌关节骨关节炎的机制研究
-
批准号:82370979
-
项目类别:面上项目
-
资助金额:48.00万元
-
批准年份:2023
-
负责人:张善勇
-
依托单位:
BRD4通过结合TEAD1调控β细胞增殖分化的机制研究
-
批准号:82370801
-
项目类别:面上项目
-
资助金额:49.00万元
-
批准年份:2023
-
负责人:李峰
-
依托单位:
22q11.2染色体微重复影响TOP3B表达并导致腭裂发生的机制研究
-
批准号:82370906
-
项目类别:面上项目
-
资助金额:48.00万元
-
批准年份:2023
-
负责人:代杰文
-
依托单位:
新生儿坏死性小肠结肠炎中去泛素化酶USP15调控ILC3分化损伤肠道粘膜屏障的致病机制研究
-
批准号:82371711
-
项目类别:面上项目
-
资助金额:49.00万元
-
批准年份:2023
-
负责人:吕志宝
-
依托单位:
生理/病理应激差异化调控肝再生的“蓝斑—中缝”神经环路机制
-
批准号:82371517
-
项目类别:面上项目
-
资助金额:49.00万元
-
批准年份:2023
-
负责人:杨立群
-
依托单位:
组蛋白乙酰化修饰ATG13激活自噬在牵张应力介导骨缝Gli1+干细胞成骨中的机制研究
-
批准号:82370988
-
项目类别:面上项目
-
资助金额:48.00万元
-
批准年份:2023
-
负责人:经典
-
依托单位:
LIPUS促进微环境巨噬细胞释放CCL2诱导尿道周围平滑肌祖细胞定植与分化的机制研究
-
批准号:82370780
-
项目类别:面上项目
-
资助金额:49.00万元
-
批准年份:2023
-
负责人:夏术阶
-
依托单位:
TNFAIP8/Hippo/SIX1轴调控软骨干细胞分化能力在颞下颌骨关节炎中的机制研究
-
批准号:82370980
-
项目类别:面上项目
-
资助金额:48.00万元
-
批准年份:2023
-
负责人:沈佩
-
依托单位:
细胞命运决定中不同蛋白水平OCT4A差异性调控CITED2转录的机制研究
-
批准号:32100597
-
项目类别:青年科学基金项目(C类)
-
资助金额:30.0万元
-
批准年份:2021
-
负责人:周艳文
-
依托单位:
小鼠肺腺鳞癌转分化类器官模型的建立及表观调控分子机制研究
-
批准号:32100593
-
项目类别:青年科学基金项目(C类)
-
资助金额:30.0万元
-
批准年份:2021
-
负责人:童欣媛
-
依托单位: