相关实验视频

Updated: May 23, 2025

Inducing Apical Periodontitis in Mice

Inducing Apical Periodontitis in Mice

Published on: August 6, 2019

ENTR1通过通过AMPK激活调节巨细胞M1极化来调节牙周炎

Xi Wang¹, Houda Gui², Chenghang Liu¹

¹Department of Prosthodontics, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, No.44-1 Wenhua Road West, 250012 Jinan, Shandong, China.

|March 7, 2025

概括

内基因相关的贩运调节剂1 (ENTR1) 抑制M1巨细胞的两极分化,通过增强AMPK酸化来减少牙周炎和骨质损失. 这为牙周炎管理提供了一个新的治疗目标.

科学领域:

口腔生物学口腔生物学
免疫学免疫学免疫学
再生医学是一种再生医学.

背景情况:

牙周炎是一种由微生物失衡和宿主免疫反应驱动的慢性炎症性疾病.
巨细胞在牙周炎的发病过程中起着至关重要的作用.
在牙周炎中,内基因相关贩运调节剂1 (ENTR1) 的功能尚不清楚.

研究的目的:

调查ENTR1在牙周炎期间巨细胞极化中的作用.
阐明ENTR1行动的基本机制.
评估ENTR1在牙周组织再生中的治疗潜力.

主要方法:

建立了一个绑定诱导的牙周炎小鼠模型.
评估了ENTR1表达和巨细胞极化标志物,使用qRT-PCR,西斑,ELISA和流细胞计.
通过微型CT和组织学染色评估了牙周骨的再吸收.
通过共免疫沉研究ENTR1-AMPK相互作用,并与AMPK抑制剂验证.

主要成果:

在牙周炎模型中,ENTR1表达减少.
过度表达ENTR1减少了M1巨细胞两极分化和骨质损失,而敲击则加剧了这些影响.
ENTR1与AMPK酸化相互作用并增强了AMPK酸化.
抑制AMPK部分逆转了ENTR1的保护作用.

结论:

ENTR1抑制了M1巨细胞的两极分化,并减轻了牙周炎引起的骨质损失.
ENTR1通过增强AMPK酸化来起作用.
在牙周炎的预防和治疗中,ENTR1是潜在的治疗点.

关键词:

这就是AMPKK.进入1 进入1 进入1 炎症炎症是一种炎症.巨细胞的两极分化牙周病是指牙周病的发生.

更多相关视频

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

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages

Published on: June 23, 2013

相关概念视频

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

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...