通过在表观遗传上增加p66Shc表达,SAHA抑制了肺纤维细胞激活
Yiheng Dong1, Jieting Peng2, Xiangyu Zhang1
1Department of Geriatrics The Second Xiangya Hospital, Central South University Changsha Hunan China.
Aging medicine (Milton (N.S.W))
|January 8, 2025
概括
苏贝罗伊兰利化酸 (SAHA) 通过表观遗传变化增加p66Shc和线粒体ROS,从而降低肺纤维细胞激活. 沉默p66Shc可以逆转这些有益的影响.
科学领域:
- 肺部医学 肺部医学
- 细胞生物学 细胞生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
背景情况:
- 肺纤维细胞激活是肺纤维化的一个关键过程.
- 对于p66Shc在肺纤维细胞激活及其SAHA调节中的作用,需要进一步研究.
研究的目的:
- 为了研究氨酸 (SAHA) 对肺纤维细胞激活的作用.
- 检查p66Shc在SAHA介导的肺纤维细胞激活调节中的作用.
主要方法:
- 通过使用TGF-β诱导的MRC-5肺纤维细胞建立了体外肺纤维化模型.
- 细胞增殖,迁移,基因表达,蛋白质水平,线粒体ROS和基因组修饰在SAHA治疗和/或p66Shc沉默后被评估.
- 技术包括西方斑点,免疫光,米托-SOX测定和ChIP测定.
主要成果:
- 在TGF-β诱导的肺纤维细胞中,SAHA抑制了纤维化标志物 (原I,α-SMA) 的增殖,迁移和表达.
- SAHA增加了p66Shc表达和线粒体ROS生成.
- 抑制p66Shc可以逆转SAHA的抑制作用.
- 在p66Shc基因区域中,SAHA增强了活跃的组素标记物 (H3K9Ac,H3K4Me3).
结论:
- 萨哈减轻了肺纤维细胞的激活和迁移.
- 这种效应是由增加的p66Shc表达和线粒体ROS生成的介导.
- 基因组3的表观遗传修饰与SAHA的作用机制有关.
关键词:
萨哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈哈基斯顿基因基因基因基因的修改肺部纤维细胞细胞.p66Shccc 在线阅读肺部纤维化 肺部纤维化更多相关视频
13:59A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
Published on: August 12, 2018
8.1K
10:26Assessment of Mitochondrial Health in Cancer-Associated Fibroblasts Isolated from 3D Multicellular Lung Tumor Spheroids
Published on: October 21, 2022
1.9K
相关概念视频
01:20The JAK-STAT Signaling Pathway
8.7K
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...
8.7K
01:09Introduction to Fibroblasts
3.0K
Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...
3.0K
01:20Chronic Obstructive Pulmonary Disease-II: Pathophysiology
2.7K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Chronic Inflammation
2.7K
01:01Regulation of Hematopoietic Stem Cells
3.1K
All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
3.1K
01:16TGF - β Signaling Pathway
7.2K
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...
7.2K