Mammary Epithelial Cell-Derived Exosomal miR-221-3p Regulates Macrophage Polarization by Targeting Igf2bp2 during Mastitis

微泡 巨噬细胞极化 乳腺炎 生物 巨噬细胞 发病机制 小RNA 细胞生物学 体内 电池类型 免疫学 细胞 体外 微生物学 基因 生物化学 遗传学
作者
Zhong‐Hao Ji,Fei Gao,Wen‐Yin Xie,Hongyu Wu,Wenzhi Ren,Bao Yuan
出处
期刊:Journal of Agricultural and Food Chemistry [American Chemical Society]
卷期号:71 (40): 14742-14757 被引量:3
标识
DOI:10.1021/acs.jafc.3c03350
摘要

Mastitis affects the milk quality and yield and is the most expensive disease in dairy cows. Elucidation of the pathogenesis of mastitis is of great importance for disease control. As a medium of intercellular communication, exosomes play key roles in various inflammatory diseases by regulating macrophage polarization. However, the molecular factors in exosomes that mediate the intercellular communication between mammary epithelial cells and macrophages during mastitis remain to be further explored. In this study, we isolated and identified mammary epithelial cell-derived exosomes from a lipopolysaccharide (LPS)/lipoteichoic acid (LTA)-induced mastitis cell model, and we demonstrated that exosomes from LPS/LTA-stimulated mammary epithelial cells promote M1-type macrophage polarization in vivo and in vitro. Based on the results of high-throughput sequencing, we constructed a differential miRNA (microRNA) expression profile of exosomes and demonstrated that miR-221-3p was highly expressed. Furthermore, in vivo and in vitro experiments, combined with coculture experiments and fluorescence tracing, showed that high miR-221-3p expression promoted M1-type macrophage polarization, demonstrating the transcellular role of miR-221-3p. Mechanistically, dual luciferase reporter gene assays and rescue assays showed that miR-221-3p regulated macrophage polarization by targeting Igf 2 bp 2. The results of this study will deepen our understanding of the pathogenesis of mastitis, and the molecular regulatory axis that was established in this study is expected to be a target for mastitis treatment.
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
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
1秒前
爱听歌的夜绿完成签到,获得积分10
1秒前
xiaoyi完成签到,获得积分10
1秒前
crycat发布了新的文献求助10
2秒前
3秒前
柴胡完成签到,获得积分10
4秒前
科研通AI6.2的应助被everestsnow采纳,获得100
5秒前
张二哈完成签到,获得积分10
5秒前
Treasure完成签到,获得积分10
6秒前
mi发布了新的文献求助10
6秒前
YU完成签到,获得积分10
7秒前
syz1209完成签到,获得积分20
8秒前
FashionBoy的应助被xingsi采纳,获得10
8秒前
8秒前
FashionBoy的应助被liu采纳,获得10
8秒前
Tito完成签到,获得积分10
10秒前
10秒前
CipherSage的应助被哈哈哈采纳,获得10
10秒前
丘比特的应助被柔弱的道消采纳,获得10
10秒前
常常完成签到,获得积分10
10秒前
11秒前
慕青的应助被haq0324采纳,获得10
12秒前
自信的小鸽子完成签到,获得积分10
12秒前
彭于晏的应助被清秀嚓茶采纳,获得10
12秒前
Aurorademon完成签到,获得积分10
13秒前
隐形的星月完成签到,获得积分20
13秒前
传奇3的应助被jr采纳,获得10
14秒前
Treasure发布了新的文献求助10
14秒前
14秒前
aaa发布了新的文献求助10
15秒前
科研通AI6.2的应助被crycat采纳,获得10
16秒前
Preseverance完成签到,获得积分10
17秒前
17秒前
月儿小虾发布了新的文献求助10
17秒前
19秒前
QW由于求助违规,被管理员扣积分30
21秒前
xixi发布了新的文献求助10
21秒前
22秒前
invisight的应助被枫落三千院采纳,获得10
22秒前
Orange的应助被优秀傲旋采纳,获得10
24秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Essentials of Carbohydrate Chemistry and Biochemistry, 4th Edition 1000
Электротехническая система магнитожидкостной герметизации валов регулируемых электродвигателей 800
日本語と中国語及びチベット・ビルマ語の語源関連性に関する分析 800
Practical Manual of Forensic Psychophysiology: Methodology, Execution, and Fields of Application 800
Holistic Discourse Analysis, Second Edition by Robert E. Longacre 666
The Basics of Practical Optimization, Second Edition 600
热门求助领域 (近24小时)
化学 材料科学 医学 生物 计算机科学 工程类 纳米技术 有机化学 物理 生物化学 化学工程 内科学 复合材料 催化作用 心理学 人工智能 细胞生物学 光电子学 无机化学 量子力学
热门帖子
关注 科研通微信公众号,转发送积分 7966479
求助须知:如何正确求助?哪些是违规求助? 9434581
关于积分的说明 21030279
捐赠科研通 7543497
什么是DOI,文献DOI怎么找? 3372076
关于科研通互助平台的介绍 2507427
邀请新用户注册赠送积分活动 2404648