已入深夜,您辛苦了!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!祝你早点完成任务,早点休息,好梦!

miR-20a-5p is enriched in hypoxia-derived tubular exosomes and protects against acute tubular injury

急性肾损伤 微泡 体外 细胞凋亡 小RNA 体内 外体 肌酐 缺氧(环境) 肾缺血 药理学 急性肾小管坏死 再灌注损伤 医学 缺血 癌症研究 细胞生物学 化学 生物 内科学 生物化学 氧气 有机化学 生物技术 基因
作者
Wei Yu,Honghui Zeng,Junzhe Chen,Sha Fu,Qiuyan Huang,Yuanyuan Xu,Anping Xu,Hui‐Yao Lan,Ying Tang
出处
期刊:Clinical Science [Portland Press]
卷期号:134 (16): 2223-2234 被引量:32
标识
DOI:10.1042/cs20200288
摘要

Abstract Exosomes have been shown to effectively regulate the biological functions of target cells. Here, we investigated the protective effect and mechanism of hypoxia-induced renal tubular epithelial cells (TECs)-derived exosomes on acute tubular injury. We found that in vitro hypoxia-induced tubular exosomes (Hy-EXOs) were protective in acute tubular injury by promoting TECs proliferation and improving mitochondrial functions. By using exosome miRNA sequencing, we identified miR-20a-5p was abundant and was a key mechanism for the protective effect of Hy-EXOs on tubular injury as up-regulation of miR-20a-5p enhanced but down-regulation of miR-20a-5p inhibited the protective effect of Hy-EXOs on tubular injury under hypoxia conditions. Further study in a mouse model of ischemia–reperfusion-induced acute kidney injury (IRI-AKI) also confirmed this notion as pre-treating mice with the miR-20a-5p agomir 48 h prior to AKI induction was capable of inhibiting IRI-AKI by lowering serum levels of creatinine and urea nitrogen, and attenuating the severity of tubular necrosis, F4/80(+) macrophages infiltration and vascular rarefaction. Mechanistically, the protective effect of miR-20a-5p on acute kidney injury (AKI) was associated with inhibition of TECs mitochondrial injury and apoptosis in vitro and in vivo. In conclusion, miR-20a-5p is enriched in hypoxia-derived tubular exosomes and protects against acute tubular injury. Results from the present study also reveal that miR-20a-5p may represent as a novel therapy for AKI.
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
闵卷完成签到,获得积分10
刚刚
朴素飞薇完成签到 ,获得积分10
1秒前
Hello应助顺利的曼寒采纳,获得10
3秒前
程风破浪发布了新的文献求助10
3秒前
伊森xay发布了新的文献求助10
5秒前
6秒前
7秒前
独特灵完成签到 ,获得积分10
11秒前
疯狂的丑发布了新的文献求助10
11秒前
12秒前
中医红发布了新的文献求助10
13秒前
zzq发布了新的文献求助30
14秒前
小二郎应助faaami采纳,获得10
16秒前
zzq完成签到,获得积分20
19秒前
小西完成签到 ,获得积分10
21秒前
Rain完成签到,获得积分20
21秒前
风生发布了新的文献求助10
22秒前
SciGPT应助耍酷夜阑采纳,获得20
23秒前
24秒前
张泽崇应助不学石油采纳,获得20
24秒前
25秒前
桐桐应助huanhuan采纳,获得10
27秒前
赫连哲瀚发布了新的文献求助10
28秒前
zxcvb666发布了新的文献求助10
31秒前
无限西装发布了新的文献求助10
32秒前
34秒前
远离焦绿完成签到 ,获得积分10
35秒前
39秒前
sparrow完成签到,获得积分10
41秒前
Jasper应助科研通管家采纳,获得10
43秒前
43秒前
脑洞疼应助科研通管家采纳,获得10
43秒前
李爱国应助科研通管家采纳,获得10
43秒前
完美世界应助科研通管家采纳,获得10
43秒前
我是老大应助科研通管家采纳,获得10
43秒前
43秒前
传奇3应助科研通管家采纳,获得20
43秒前
43秒前
开放磬完成签到,获得积分10
44秒前
huanhuan发布了新的文献求助10
48秒前
高分求助中
Manual of Clinical Microbiology, 4 Volume Set (ASM Books) 13th Edition 1000
Sport in der Antike 800
De arte gymnastica. The art of gymnastics 600
少脉山油柑叶的化学成分研究 530
Mechanical Methods of the Activation of Chemical Processes 510
Electronic Structure Calculations and Structure-Property Relationships on Aromatic Nitro Compounds 500
Berns Ziesemer - Maos deutscher Topagent: Wie China die Bundesrepublik eroberte 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 有机化学 工程类 生物化学 纳米技术 物理 内科学 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 电极 光电子学 量子力学
热门帖子
关注 科研通微信公众号,转发送积分 2418057
求助须知:如何正确求助?哪些是违规求助? 2109959
关于积分的说明 5337019
捐赠科研通 1837142
什么是DOI,文献DOI怎么找? 914864
版权声明 561100
科研通“疑难数据库(出版商)”最低求助积分说明 489259