相关实验视频

Updated: Jul 21, 2025

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Published on: March 7, 2022

RNA甲基化读取蛋白YTHDF2通过通过m⁶A修改向下调节BNIP3来缓解心肌缺血-再输液损伤

Xinyong Cai¹, Pengtao Zou¹, Lang Hong¹

¹Department of Cardiology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, No. 92, Aiguo Road, Donghu District, Nanchang, Jiangxi, 330006, People's Republic of China.

|July 27, 2023

概括

RNA甲基化阅读器YTHDF2通过减少BNIP3驱动的线粒细胞衰变来防止心肌缺血-反损伤 (MIRI). 抑制YTHDF2在MIRI期间改善心脏损伤和细胞死亡.

科学领域:

心血管生物学心血管生物学
线粒体生物学线粒体生物学
细胞死亡途径细胞死亡途径

背景情况:

缺氧诱导的线粒体功能障碍和细胞死亡与心肌细胞有关.
在心肌缺血-再输损伤 (MIRI) 中BNIP3介导的线粒的作用尚不清楚.

研究的目的:

在MIRI中研究BNIP3调节的线粒的机制.
探索RNA甲基化阅读器YTHDF2在调节BNIP3表达中的作用及其对MIRI的影响.

主要方法:

鼠心肌细胞 (H9c2细胞) 经过低氧/低氧化 (H/R) 和转染.
实体MIRI模型在老鼠中建立,并进行功能增益测试.
评估了细胞活力,细胞亡,心脏功能,心肌梗塞区域和分子标记 (CK-MB,cTnI,LDH,ROS,MDA,SOD,p62,LC3 II/LC3 I) 的情况.

主要成果:

H/R治疗诱导了心肌细胞损伤,亡和线粒细胞衰变,通过降低BNIP3或升高YTHDF2的调节来减轻这些损伤.
在MIRI中,YTHDF2识别了甲基化BNIP3,调解了其表达,从而抑制了线粒和心肌损伤.
过度表达BNIP3逆转了YTHDF2在H/R诱导的损伤和线粒的保护作用.

结论:

通过m6A修饰,YTHDF2通过降低BNIP3表达的调节来改善MIRI,从而抑制过度的线粒.
针对YTHDF2/BNIP3轴为MIRI提供了一个潜在的治疗策略.

关键词:

在BNIP3中,BNIP3是BNP3.线粒细胞衰变 (mitophagy) 是一种神经衰变.心肌缺血再输血损伤的心肌缺血这就是YTHDF2的原因.m6A 修改的修改

更多相关视频

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation

Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation

Published on: January 10, 2025

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model

Published on: October 27, 2020

相关概念视频

Epigenetic Regulation

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.

Spreading of Chromatin Modifications

Spreading of Chromatin Modifications

The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer...

Nonsense-mediated mRNA Decay

Nonsense-mediated mRNA Decay

The Upf proteins that carry out nonsense-mediated decay (NMD) are found in all eukaryotic organisms, including humans. Each protein has an individual role, but they need to work in collaboration. Upf1 is an ATP-dependent RNA helicase that unwinds the RNA helix. Because Upf1 can unwind any RNA, Upf2 and Upf3 are required to help Upf1 discriminate between nonsense and normal mRNAs.
Usually, Upf3 binds to an Exon Junction Complex (EJC) at mRNA splice sites. If a ribosome fully translates the mRNA,...

Biosynthesis of Nucleic Acids

Biosynthesis of Nucleic Acids

Nucleic acid biosynthesis is a fundamental biochemical process that produces the purine and pyrimidine nucleotides essential for DNA and RNA synthesis. This pathway maintains a balanced nucleotide pool, preventing imbalances that could jeopardize genetic integrity and cellular function. Given the crucial role of nucleotides, their synthesis is tightly regulated to ensure proper cellular homeostasis.Purine BiosynthesisThe biosynthesis of purine nucleotides begins with ribose-5-phosphate, a...

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...

Histone Modification

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone...