相关实验视频
Updated: Jun 24, 2025

10:26
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
12.1K
长跨基因非编码RNA 01126激活IL-6/JAK2/STAT3通路,促进牙周炎的发病
Song Tang1,2,3, Yi Zhong4, Jie Li1,2,3
1College of Stomatology, Chongqing Medical University, Chongqing, China.
Oral diseases
|June 9, 2024
概括
长跨基因非编码RNA 01126 (LINC01126) 通过海绵化miR-655-3p促进牙周炎,激活IL-6/JAK2/STAT3通路. 这一发现为牙周炎病原和潜在的治疗点提供了新的见解.
科学领域:
- 口腔生物学和疾病机制
- 分子生物学和RNA研究.
- 炎症和免疫学 炎症和免疫学
背景情况:
- 牙周炎显著影响口腔健康和整体幸福感.
- 在牙周炎组织中观察到长跨基因非编码RNA 01126 (LINC01126) 的异常表达.
研究的目的:
- 调查LINC01126在牙周炎病变发生过程中的作用和潜在机制.
- 探索LINC01126,miR-655-3p和IL-6/JAK2/STAT3信号通路之间的相互作用.
主要方法:
- 使用人类牙纤维细胞 (HGFs) 建立了一个炎症模型.
- 采用细胞活力测试 (CCK-8),迁移测试 (伤口愈合) 和流动细胞测量来评估细胞功能.
- 利用生物信息学预测和实验验证,确认LINC01126,miR-655-3p和IL-6之间的结合点.
- 分析的临床样本使用血素-氨酸 (H&E) 和免疫组织化学 (IHC) 染色.
主要成果:
- LINC01126沉默降低了炎症,亡,并增强了HGFs中的迁移.
- LINC01126 作为 miR-655-3p 的分子海绵,抑制其与 IL-6 mRNA 的相互作用.
- 这种相互作用促进炎症,并激活JAK2/STAT3通路.
- 临床样本显示miR-655-3p表达减少,并在牙周炎组织中激活IL-6/JAK2/STAT3信号.
结论:
- LINC01126 作为 miR-655-3p.p. 的内源性竞争性RNA 起作用.
- 通过激活IL-6/JAK2/STAT3通路,LINC01126促进牙周炎的发生.
- 这些发现突出了LINC01126作为牙周炎的潜在治疗点.
相关概念视频
The JAK-STAT Signaling Pathway
8.8K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
8.8K
TGF - β Signaling Pathway
7.3K
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...
7.3K
Role Of Notch Signalling In Intestinal Stem Cell Renewal
2.1K
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.1K
NF-κB-dependent Signaling Pathway
7.4K
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...
NF-κB-dependent Signaling Mechanism
The...
7.4K
T Cell Types and Functions
1.0K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
1.0K
MAPK Signaling Cascades
5.4K
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.4K

