miR-331-depleted exosomes derived from injured endometrial epithelial cells promote macrophage activation during endometritis

促炎细胞因子 微泡 子宫内膜炎 巨噬细胞 炎症 下调和上调 细胞生物学 外体 癌症研究 脂多糖 免疫学 生物 小RNA 生物化学 怀孕 体外 遗传学 基因
作者
Kangfeng Jiang,Yajing Chen,Kui Wang,Yang Yang,Shumin Sun,Jing Yang,Xiaobing Li
出处
期刊:International Journal of Biological Macromolecules [Elsevier]
卷期号:279: 134967-134967
标识
DOI:10.1016/j.ijbiomac.2024.134967
摘要

Exosomes are natural carriers of biological macromolecules that are involved in the pathogenesis of a wide variety of inflammatory diseases. The purpose of this study was to investigate the role of exosomes derived from injured endometrial epithelial cells (EECs) in the development of endometritis. We isolated exosomes derived from LPS-injured EECs and identified these exosomes as proinflammatory mediators that can be internalized by macrophages and thus induce proinflammatory macrophage activation. We further found that miR-331 expression was sharply downregulated in exosomes derived from LPS-injured EECs and that macrophages treated with these exosomes also presented a lower level of miR-331. Importantly, the pathogenic role of exosomal miR-331 in promoting endometrial inflammation was revealed by the ability of adoptively transferred EECs-derived exosomes to cause macrophage activation, and this was reversed by miR-331 overexpression. Mechanistically, overexpression of miR-331 in macrophages mitigated NF-κB p65 phosphorylation by inhibiting the Notch1/IKKα pathway, which in turn curbed macrophage activation. In vivo assays further unveiled that miR-331 expression is negatively correlated with proinflammatory macrophage activation and that miR-331 upregulation markedly slowed disease progression in mice with endometritis. The exosome/miR-331/Notch1 axis plays a critical pathological role in endometrial inflammation, representing a new therapeutic target for endometritis.
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
刚刚
寻觅发布了新的文献求助10
1秒前
1秒前
喵喵7完成签到 ,获得积分10
1秒前
1秒前
TRz发布了新的文献求助10
1秒前
Kabutack完成签到,获得积分10
1秒前
2秒前
2秒前
呜呼啦呼发布了新的文献求助10
3秒前
喜欢你很久了关注了科研通微信公众号
3秒前
wren完成签到,获得积分10
3秒前
芝芝霉霉完成签到,获得积分10
4秒前
sssss发布了新的文献求助10
4秒前
大傻春完成签到 ,获得积分10
5秒前
炙热的桐发布了新的文献求助10
5秒前
laura发布了新的文献求助10
6秒前
7秒前
犹豫嚣发布了新的文献求助10
7秒前
买尔孜亚发布了新的文献求助30
7秒前
多睡会儿发布了新的文献求助10
8秒前
张_5238完成签到,获得积分10
8秒前
8秒前
9秒前
JamesPei应助温暖从菡采纳,获得10
9秒前
9秒前
CodeCraft应助啊饭采纳,获得10
10秒前
InfoNinja应助快乐滑板采纳,获得50
10秒前
失眠的以蓝完成签到,获得积分20
10秒前
lushanxihai完成签到,获得积分10
11秒前
Alina1874完成签到,获得积分10
11秒前
123发布了新的文献求助10
11秒前
11秒前
汉堡包应助wtf采纳,获得10
13秒前
curtisness应助可可可采纳,获得10
13秒前
Freja完成签到,获得积分10
14秒前
David发布了新的文献求助10
14秒前
14秒前
JinwenShi完成签到,获得积分10
14秒前
小小雨泪完成签到,获得积分10
16秒前
高分求助中
Evolution 10000
Sustainability in Tides Chemistry 2800
The Young builders of New china : the visit of the delegation of the WFDY to the Chinese People's Republic 1000
юрские динозавры восточного забайкалья 800
English Wealden Fossils 700
Diagnostic immunohistochemistry : theranostic and genomic applications 6th Edition 500
Chen Hansheng: China’s Last Romantic Revolutionary 500
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 3148410
求助须知:如何正确求助?哪些是违规求助? 2799502
关于积分的说明 7835226
捐赠科研通 2456813
什么是DOI,文献DOI怎么找? 1307424
科研通“疑难数据库(出版商)”最低求助积分说明 628189
版权声明 601655