Analysis of GFP Transgenes in Odontoblast in Differentiation

成牙本质细胞分化过程中 GFP 转基因的分析

基本信息

批准号：
10453476
负责人：
Mina Mina
金额：
$ 36.9万
依托单位：
UNIVERSITY OF CONNECTICUT SCH OF MED/DNT
依托单位国家：
美国
项目类别：
财政年份：
2006
资助国家：
美国
起止时间：
2006-07-01 至 2023-08-05
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10453476
关键词：
Address Biological Process Cells Cessation of life Characteristics Collagen Fiber Complex DSPP gene Dental Pulp Dental caries Dentin Dentinogenesis Development Endodontics Environment Event Genetic Transcription Goals Histologic Impairment Inflammation Injury Lead Light Mediating Mesenchymal Stem Cells Minerals Molecular Mus Natural regeneration Odontoblasts Osteoblasts Osteogenesis Physiological Population Process Proteins Raman Spectrum Analysis Signal Pathway Signal Transduction Site Structure Testing Thinness Tissues Transgenes Trauma Tubular formation bone bone sialoprotein calcification design experimental study gain of function healing improved in vivo injured insight loss of function migration mineralization nestin protein novel osteoblast differentiation osteogenic osteopontin polarized light progenitor programs recruit regeneration potential regenerative repaired second harmonic generation imaging spectroscopic imaging stem cell differentiation treatment strategy

项目摘要

PROJECT SUMMARY / ABSTRACT Reparative dentinogenesis occurs after intense injury that leads to odontoblast death (i.e., deep caries or pulp exposure). During this process, signaling factors sequestered in the dentin matrix and pulp-supportive tissue are released and activate the recruitment, migration of resident Mesenchymal Stem cells (MSCs) in dental pulp to the site of injury. At the site of injury, these MSCs differentiate and give rise to cells secreting reparative dentin, also called osteodentin. Reparative dentin is a thin band of poorly organized mineralized tissue containing a mixture of non-columnar odontoblast-like and osteoblast-like cells. Although the reparative dentin/osteo-dentin provides an impermeable hard-tissue barrier to the dental pulp, its histological and molecular characteristic is very different from physiological dentin and cannot be considered a true regeneration of tubular dentin devoid of osteoblasts. The overall goal of proposed studies is to test the hypothesis that signaling pathways induced by trauma/inflammation to the pulp during pulp exposures results in abnormal and sustained activation of Runx2 in dental pulp. The sustained activation of Runx2 leads to impaired odontoblasts differentiation and accumulation of osteoblasts at the site of injury and together contribute to the formation of atubular and poorly organized mineralized reparative dentin. To address this sequence, we will use examine the effects of conditional modulation of levels of Runx2 (loss of function and gain of functions) on the late stages of odontoblast and osteoblasts differentiation. Three specific aims have been proposed. Experiments in Aim #1 and Aim 2 will examine the effects of conditional modulation of levels of Runx2 (loss of function and gain of functions) in odontoblasts and osteoblasts on the late stages of odontoblast (Aim 1) and osteoblast (Aim 2) differentiation during reparative dentinogenesis in vivo and during mineralization of primary pulp cultures. Experiments in Aim #3 will examine the effects of impaired odontoblast differentiation and accumulation of osteoblasts during reparative dentinogenesis the organization of collagen fibers and tubular vs. atubular dentin. Ultimately, the results of this study will provide a better understanding of mechanisms leading to reparative dentinogenesis and will be critical for the development of improved treatments for vital pulp therapy and improved dentin regeneration.

项目摘要 /摘要修复性牙本质发生是在剧烈损伤后发生的，导致牙本质细胞死亡（即，龋齿或果肉接触）。在此过程中，信号传导因子在牙本质基质和纸浆支持组织中隔离释放并激活牙齿牙髓中驻留间充质干细胞（MSC）的招募，迁移到受伤部位。在受伤部位，这些MSC分化并引起分泌率的细胞牙本质，也称为骨丁丁。修复性牙本质是一条细小的矿物质组织的薄带包含非柱状牙胶样细胞和成骨细胞样细胞的混合物。虽然是修复的牙本质/骨丁丁为牙髓，其组织学和分子特征与生理牙本质有很大不同，不能被认为是正确的管状牙本质的再生，没有成骨细胞。拟议研究的总体目标是测试假设在果肉暴露期间因创伤/炎症引起的创伤/炎症引起的信号传导途径在牙髓中Runx2的异常和持续激活中。 runx2的持续激活导致牙本质细胞损害可在伤害部位分化和成骨细胞的积累，一起有助于形成较低的矿物质修复牙本质。解决这个问题序列，我们将使用检查Runx2级别的条件调制的影响（功能损失和功能的增益）在Odontoblast和成骨细胞的晚期分化。三个具体目标已提出。 AIM＃1和AIM 2中的实验将检查有条件调制的效果 odontoblasts的odontoblasts和成骨细胞中的runx2（功能丧失和功能增益）（AIM 1）和成骨细胞（AIM 2）在体内和在体内和期间的牙线发生过程中的分化原发性纸浆培养物的矿化。 AIM＃3中的实验将检查Odontoblast受损的影响在修复性牙本质发生过程中，成骨细胞的分化和积累胶原蛋白的组织纤维和管状牙齿牙本质。最终，这项研究的结果将更好地理解导致修复性牙本质发生的机制，对于改善的发展至关重要重要的纸浆治疗和改善牙本质再生的治疗方法。

项目成果

期刊论文数量（6）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Characterization of stem and progenitor cells in the dental pulp of erupted and unerupted murine molars.

DOI：
10.1016/j.bone.2010.02.019
发表时间：
2010-06
期刊：
BONE
影响因子：
4.1
作者：
Balic, Anamaria;Aguila, H. Leonardo;Caimano, Melissa J.;Francone, Victor P.;Mina, Mina
通讯作者：
Mina, Mina

Activation of αSMA expressing perivascular cells during reactionary dentinogenesis.

DOI：
10.1111/iej.12983
发表时间：
2019-01
期刊：
International endodontic journal
影响因子：
5
作者：
Vidovic-Zdrilic I;Vijaykumar A;Mina M
通讯作者：
Mina M

Generation and characterization of DSPP-Cerulean/DMP1-Cherry reporter mice.

DSPP-Cerulean/DMP1-Cherry 报告小鼠的生成和表征。

DOI：
10.1002/dvg.23324
发表时间：
2019
期刊：
Genesis (New York, N.Y. : 2000)
影响因子：
0
作者：
Vijaykumar,Anushree;Ghassem-Zadeh,Sean;Vidovic-Zdrilic,Ivana;Komitas,Karren;Adameyko,Igor;Krivanek,Jan;Fu,Yu;Maye,Peter;Mina,Mina
通讯作者：
Mina,Mina

The BMP and FGF pathways reciprocally regulate odontoblast differentiation.

BMP 和 FGF 途径相互调节成牙本质细胞分化。