miR-191-5p通过向EGR1细胞减弱了细胞核中TNF-α诱导的炎症
Zeyu Yang1, Lin Li2, Rubing Lin3
1Department of Orthopedics, Taizhou Municipal Hospital, Taizhou, 318000, China.
Journal of orthopaedic surgery and research
|November 5, 2025
概括
微RNA-191-5p (miR-191-5p) 在椎间盘退化 (IVDD) 中起着至关重要的作用. 较低的miR-191-5p水平与IVDD进展有关,其恢复可以通过向EGR1.1来缓解退化.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 整形外科 整形外科 整形外科
背景情况:
- 椎间盘退化 (IVDD) 是一种常见的骨科疾病,导致腰部疼痛,机制尚不清楚.
- 微RNAs (miRNAs) 的失调越来越多地与IVDD的发病有关.
- 这项研究研究了miR-191-5p在IVDD中的特定作用.
研究的目的:
- 阐明miR-191-5p在椎间盘退化 (IVDD) 中的分子机制.
- 在IVDD中确定miR-191-5p,EGR1和细胞外矩阵 (ECM) 之间的关系.
主要方法:
- 用于诱导IVDD的瘤缩因子-α (TNF-α) 的细胞模型.
- 使用RT-qPCR,双化酶记者分析,CCK-8,Transwell和ELISA来分析miR-191-5p,EGR1,ECM标记物,细胞活力,迁移和炎症因素.
主要成果:
- 在IVDD患者中,miR-191-5p水平显著降低,与退行症严重程度相反相关.
- 过度表达miR-191-5p增加了原II,降低了MMP-13/MMP-3,增强了细胞活力/迁移,并减少了细胞亡和炎症性细胞因子 (IL-1β,IL-18).
- 这些效应取决于EGR1.1的下调.
结论:
- miR-191-5p通过增强细胞活力和迁移来减轻IVDD的进展.
- miR-191-5p通过负调节EGR1.1,抑制细胞外基质降解,亡和炎症.
- 向miR-191-5p代表了IVDD的潜在治疗策略.
相关概念视频
NF-κB-dependent Signaling Pathway
9.7K
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...
9.7K
T Cell Types and Functions
2.1K
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...
2.1K
TGF - β Signaling Pathway
10.4K
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...
10.4K
Receptor Downregulation in MVBs
2.7K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...
2.7K
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
470
Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
470


