相关实验视频

Updated: Jun 22, 2025

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

平板3/NUDT21/NF-κB轴介导P. gingivalis-抑制的水泥细胞矿化

Hantao Huang¹, Li Ma^1,2, Xiaoxuan Wang^1,2

¹State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.

|July 3, 2024

概括

Porphyromonas gingivalis 通过降低 Platr3 的表达,抑制了水泥细胞矿化. 恢复Platr3 (多能性相关转录3) 通过NUDT21-NF-κB通路抵消这种效应,为牙周炎提供潜在的治疗标.

科学领域:

口腔生物学口腔生物学
分子生物学分子生物学
牙周病学牙周病学

背景情况:

Porphyromonas gingivalis 是牙周炎和牙周炎的关键病原体.
长非编码RNAs (lncRNAs) 影响细胞矿化和炎症反应.
在P. gingivalis诱导的水泥细胞功能障碍中,lncRNAs的作用尚不清楚.

研究的目的:

调查lncRNA,特别是Platr3在P. gingivalis刺激的水泥细胞矿化中的作用和机制.
为了阐明涉及P. gingivalis介导的水泥细胞功能抑制的分子途径.

主要方法:

在体内使用C57BL/6小鼠 (健康,AP,AP + P. gingivalis) 进行微型CT和免疫组织化学的研究.
用P. gingivalis治疗的水泥细胞体内实验,通过qPCR和西方 blot分析基因和蛋白质表达 (Platr3,IL1B,骨质生标记物).
RNA下拉,RNA免疫沉降和RNA测序以识别Platr3相互作用蛋白和通路 (NUDT21,NF-κB).

主要成果:

活体中P. gingivalis感染促进了周周组织破坏和IL1B表达,同时抑制了Platr3.3.
在体外,P. gingivalis增加了IL1B,但降低了Platr3和骨质原生标志物在水泥细胞中的表达.
Platr3过度表达逆转了P. gingivalis诱导的矿化抑制; Platr3结合NUDT21,调节NF-κB通路.

结论:

P. gingivalis 抑制了水泥细胞矿化,部分原因是通过降低 Platr3.3 的调节.
Platr3通过与NUDT21相互作用和调节NF-κB信号通路来减轻P. gingivalis诱导的影响.
Platr3-NUDT21-NF-κB轴代表了牙周炎的潜在治疗标.

关键词:

盘子盘子盘子葡萄牙牙牙病 Porphyromonas gingivalis 这种虫害的在 NF-κBB 中.NUDT2121 裸体的时间一个水泥塑料塑料.矿物化的矿化.

更多相关视频

Accessing the Cytotoxicity and Cell Response to Biomaterials

Accessing the Cytotoxicity and Cell Response to Biomaterials

Published on: July 8, 2021

Author Spotlight: Establishing an Accurate Microhardness Testing Protocol for Craniofacial Tissues

Author Spotlight: Establishing an Accurate Microhardness Testing Protocol for Craniofacial Tissues

Published on: April 26, 2024

相关概念视频

NF-κB-dependent Signaling Pathway

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...

Co-activators and Co-repressors

Co-activators and Co-repressors

Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...

TGF - β Signaling Pathway

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...