亲爱的研友该休息了!由于当前在线用户较少,发布求助请尽量完整的填写文献信息,科研通机器人24小时在线,伴您度过漫漫科研夜!身体可是革命的本钱,早点休息,好梦!

Plasma extracellular vesicle delivery of miR-210-3p by targeting ATG7 to promote sepsis-induced acute lung injury by regulating autophagy and activating inflammation.

医学 败血症 细胞凋亡 癌症研究 微泡 药理学 急性呼吸窘迫综合征 外体 PI3K/AKT/mTOR通路 下调和上调 HMGB1
作者
Guang Li,Bo Wang,Xiangchao Ding,Xinghua Zhang,Jian Tang,Huiqing Lin
出处
期刊:Experimental and Molecular Medicine [Springer Nature]
卷期号:53 (7): 1180-1191
标识
DOI:10.1038/s12276-021-00651-6
摘要

Extracellular vesicles (EVs) can be used for intercellular communication by facilitating the transfer of miRNAs from one cell to a recipient cell. MicroRNA (miR)-210-3p is released into the blood during sepsis, inducing cytokine production and promoting leukocyte migration. Thus, the current study aimed to elucidate the role of plasma EVs in delivering miR-210-3p in sepsis-induced acute lung injury (ALI). Plasma EVs were isolated from septic patients, after which the expression of various inflammatory factors was measured using enzyme-linked immunosorbent assay. Cell viability and apoptosis were measured via cell counting kit-8 and flow cytometry. Transendothelial resistance and fluorescein isothiocyanate fluorescence were used to measure endothelial cell permeability. Matrigel was used to examine the tubulogenesis of endothelial cells. The targeting relationship between miR-210-3p and ATG7 was assessed by dual-luciferase reporter assays. The expression of ATG7 and autophagy-related genes was determined to examine autophagic activation. A sepsis mouse model was established by cecal ligation and puncture (CLP)-induced surgery. The level of miR-210-3p was highly enriched in septic EVs. MiR-210-3p enhanced THP-1 macrophage inflammation, BEAS-2B cell apoptosis, and HLMVEC permeability while inhibiting angiogenesis and cellular activity. MiR-210-3p overexpression reduced ATG7 and LC3II/LC3I expression and increased P62 expression. Improvements in vascular density and autophagosome formation, increased ATG7 expression, and changes in the ratio of LC3II/LC3I were detected, as well as reduced P62 expression, in adenovirus-anti-miR-210-3p treated mice after CLP injury. Taken together, the key findings of the current study demonstrate that plasma EVs carrying miR-210-3p target ATG7 to regulate autophagy and inflammatory activation in a sepsis-induced ALI model.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
lixuebin完成签到 ,获得积分10
8秒前
自由的梦露完成签到 ,获得积分10
1分钟前
FashionBoy应助AireenBeryl531采纳,获得10
1分钟前
2分钟前
2分钟前
3分钟前
4分钟前
李健应助心平气和采纳,获得10
4分钟前
Lucas应助可靠的寒风采纳,获得10
4分钟前
4分钟前
心平气和发布了新的文献求助10
4分钟前
5分钟前
烟花应助科研通管家采纳,获得10
5分钟前
danniers完成签到,获得积分10
5分钟前
liuqizong123发布了新的文献求助10
5分钟前
liuqizong123完成签到,获得积分10
5分钟前
5分钟前
5分钟前
5分钟前
5分钟前
嘤嘤怪完成签到 ,获得积分10
5分钟前
6分钟前
Wei发布了新的文献求助10
6分钟前
数学情缘完成签到 ,获得积分10
6分钟前
oracl完成签到 ,获得积分10
6分钟前
6分钟前
6分钟前
7分钟前
Jeriu发布了新的文献求助10
7分钟前
7分钟前
Jeriu完成签到,获得积分10
7分钟前
Wei发布了新的文献求助10
7分钟前
Jasper应助笨笨小熊猫采纳,获得10
7分钟前
7分钟前
神说要有光完成签到,获得积分10
7分钟前
Wei发布了新的文献求助10
7分钟前
王柯文完成签到,获得积分10
7分钟前
Wei发布了新的文献求助10
8分钟前
安详跳跳糖完成签到,获得积分10
8分钟前
8分钟前
高分求助中
Evolution 10000
Sustainability in Tides Chemistry 2800
юрские динозавры восточного забайкалья 800
English Wealden Fossils 700
Diagnostic immunohistochemistry : theranostic and genomic applications 6th Edition 500
Mantiden: Faszinierende Lauerjäger Faszinierende Lauerjäger 400
PraxisRatgeber: Mantiden: Faszinierende Lauerjäger 400
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3154982
求助须知:如何正确求助?哪些是违规求助? 2805698
关于积分的说明 7865798
捐赠科研通 2463927
什么是DOI,文献DOI怎么找? 1311677
科研通“疑难数据库(出版商)”最低求助积分说明 629688
版权声明 601853