相关实验视频

Updated: Jul 10, 2025

All-optical Mechanobiology Interrogation of Yes-associated Protein in Human Cancer and Normal Cells using a Multi-functional System

All-optical Mechanobiology Interrogation of Yes-associated Protein in Human Cancer and Normal Cells using a Multi-functional System

Published on: December 20, 2021

异常的机械应力诱导的冠状细胞衰老由YAP损失介导的METTL3上调调节

Fan Yang¹, Peiqi Wang¹, Xiaomeng Dong¹

¹State Key Laboratory of Oral Diseases and National Clinical Research Center for Oral Diseases, Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

|November 20, 2023

概括

异常的机械压力通过诱导状细胞衰老,导致关节骨关节炎 (TMJOA). 抑制N⁶-甲基氨酸 (m⁶A) 修饰可以逆转这种衰老并治疗TMJOA.

科学领域:

生物医学工程生物医学工程
分子生物学分子生物学
史诗转录组学史诗转录组学

背景情况:

异常的机械压力是关节骨关节炎 (TMJOA) 的主要危险因素.
了解机械压力诱导的状细胞衰老的分子机制对于TMJOA治疗至关重要.

研究的目的:

研究如何异常的机械压力诱导TMJOA中的冠状细胞衰老.
在这个过程中探索YES相关蛋白 (YAP) 和N⁶-甲基氨酸 (m⁶A) 修饰的作用.
评估抑制TMJOA中的m6A修饰的治疗潜力.

主要方法:

使用动物模型单边前部交叉咬伤和体外机械过载的冠状细胞.
评估了YES相关蛋白 (YAP) 对状细胞衰老的影响.
研究了YAP,甲基转移酶类似3 (METTL3) 和m⁶A修饰之间的相关性.
确定了m6A在冠状细胞衰老中的作用及其在TMJOA中的治疗作用.

主要成果:

在老鼠机械诱导的TMJOA病变中积累的衰老性红细胞.
机械过载在体外引发了冠状细胞衰老.
通过促进METTL3-依赖的m⁶A修饰,YAP缺陷调解了机械应激诱导的衰老.
抑制m⁶ 一种修改在体外和体内挽救了冠状细胞衰老,抑制了TMJOA的进展.

结论:

在TMJOA中,机械诱导的冠状细胞衰老是由YAP缺陷和METTL3依赖的m6A修饰介导的.
m⁶ 在TMJOA的发病过程中,一种修改起着至关重要的作用.
抑制m6的修改为TMJOA提供了一个有前途的治疗策略.

关键词:

细胞衰老细胞衰老冠状腺细胞冠状腺细胞骨关节炎是一种关节炎.短关节和关节的时间

更多相关视频

Real-time Visualization and Analysis of Chondrocyte Injury Due to Mechanical Loading in Fully Intact Murine Cartilage Explants

Real-time Visualization and Analysis of Chondrocyte Injury Due to Mechanical Loading in Fully Intact Murine Cartilage Explants

Published on: January 7, 2019

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Identification of Transcription Factor Regulators using Medium-Throughput Screening of Arrayed Libraries and a Dual-Luciferase-Based Reporter

Published on: March 27, 2020

相关概念视频

Abnormal Proliferation

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...

Replicative Cell Senescence

Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...

DNA Damage can Stall the Cell Cycle

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...