相关实验视频

Updated: Jun 17, 2025

Identification, Isolation, and Characterization of Fibro-Adipogenic Progenitors FAPs and Myogenic Progenitors MPs in Skeletal Muscle in the Rat

Identification, Isolation, and Characterization of Fibro-Adipogenic Progenitors FAPs and Myogenic Progenitors MPs in Skeletal Muscle in the Rat

Published on: June 9, 2021

阿迪波内克抑制了肺纤维细胞的依赖于硬度的,益纤维的激活

Julia Nemeth¹, Wioletta Skronska-Wasek², Sophie Keppler¹

¹Institute of General Physiology, Ulm University, Ulm, Germany.

American journal of physiology. Lung cellular and molecular physiology

|August 6, 2024

概括

异形性肺纤维化 (IPF) 涉及肺组织硬化,激活纤维细胞. 通过CDH13和p38MAPKγ重新激活阿迪波涅丁信号,抑制了这种激活,提供了潜在的IPF疗法.

科学领域:

肺部医学肺部医学
细胞生物学细胞生物学
生物化学生物化学

背景情况:

异形性肺纤维化 (IPF) 是一种进展性肺病,其特征是过度纤维细胞激活和细胞外基质沉积.
在IPF中增加的组织度会放大纤维细胞激活,推动疾病的进展并限制治疗选择.

研究的目的:

通过使用无偏的下一代测序,识别参与硬度依赖性肺纤维细胞激活的信号通路.
调查向皮细胞因子信号传导作为IPF治疗策略的潜力.

主要方法:

在硬基质上培养的初级肺纤维细胞 (PFs) 上进行下一代测序 (NGS) 选.
研究了在IPF纤维细胞中阿迪波涅丁信号传递,CDH13表达和p38基因激活蛋白激酶玛 (p38MAPKγ) 激活的作用.
分析了IPF捐赠者的肺组织中的基因表达和蛋白质激活.

主要成果:

在硬基质上培养的PF中,皮细胞因子信号被下调.
阿迪波涅克丁治疗抑制了人体PFs的硬度依赖激活.
亚迪波涅丁信号依赖于CDH13和p38MAPKγ;两者都在IPF肺部减少.
数据表明,阿迪波内克的信号传递抑制了亲蛋白质纤维细胞的激活.

结论:

通过CDH13和p38MAPKγ介导的阿迪波涅丁信号,抑制了肺中的profibrotic纤维细胞激活.
准阿迪波涅克丁信号级联为IPF提供了潜在的治疗途径.
调节依赖于性的纤维细胞激活可能会减缓IPF的进展.

关键词:

这就是T-cadherin.没有任何的Adiponectin.异形性肺纤维化异形性肺纤维化机械信号传输系统 p38 MAPKK 的时间.

更多相关视频

Author Spotlight: Streamlining Cell Analysis with an Innovative Protocol for Studying Spiny Mouse Models

Author Spotlight: Streamlining Cell Analysis with an Innovative Protocol for Studying Spiny Mouse Models

Published on: November 15, 2024

Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition

Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition

Published on: June 10, 2016

相关概念视频

Actin Filament Depolymerization

Actin Filament Depolymerization

Actin filaments (F-actin) are composed of actin subunits. The dissociation of actin monomers can occur from either end of F-actin. The rate of dissociation is faster from the minus-end or the pointed end, where the actin subunits exist with a bound ADP, together known as ADP-actin. The depolymerization of F-actin is aided by proteins, including the actin-depolymerizing factor (ADF) and cofilin family of proteins, gelsolin, and glia maturation factor (GMF).
In F-actin, the ADF/cofilin proteins...

Intracellular Signaling Affects Focal Adhesions

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...

Cell-matrix's Response to Mechanical Forces

Cell-matrix's Response to Mechanical Forces

In animal cells, the extracellular matrix allows cells within tissues to withstand external stresses and transmits signals from the outside of the cell to the inside. The extracellular matrix is extensive, and its composition varies between different types of tissues. For example, the reticular fibers and ground substance make up the ECM in loose connective tissue, while collagen and bone minerals make up the ECM of bone tissue.
Anchoring junctions mechanically attach a cell to the...