MiR-223-3p attenuates M1 macrophage polarization via suppressing the Notch signaling pathway and NLRP3-mediated pyroptosis in experimental autoimmune uveitis

上睑下垂 葡萄膜炎 巨噬细胞极化 Notch信号通路 免疫学 炎症体 发病机制 信号转导 自身免疫 细胞生物学 炎症 医学 癌症研究 生物 化学 巨噬细胞 免疫系统 生物化学 体外
作者
Ruyi Qu,Yuan Peng,Mengxian Zhou,Shuqin Xu,Xuewei Yin,Yan Qiu,Bin Liu,Yane Gao,Hongsheng Bi,Dadong Guo
出处
期刊:European Journal of Pharmacology [Elsevier BV]
卷期号:960: 176139-176139 被引量:6
标识
DOI:10.1016/j.ejphar.2023.176139
摘要

Autoimmune uveitis is an intraocular inflammatory disease with a high blindness rate in developed countries such as the United States. It is pressing to comprehend the pathogenesis of autoimmune uveitis and develop novel schemes for its treatment. In the present research, we demonstrated that the Notch signaling pathway was activated, and the level of miR-223-3p was significantly reduced in rats with experimental autoimmune uveitis (EAU) compared with the level of normal rats. To investigate the relationship between miR-223-3p and Notch signaling, EAU rats received miR-223-3p-carrying lentivirus, miR-223-3p vector-carrying lentivirus (miR-223-3p-N), and γ-secretase inhibitor (DAPT), respectively. The results of Q-PCR, immunological experiments, and flow cytometry analysis all support the hypothesis that both miR-223-3p and DAPT, a Notch signaling pathway inhibitor, had similar inhibitory effects on the EAU pathological process. That is to say, they could both inhibit the activation of the Notch signaling pathway via modulating recombination signal binding protein-Jκ (RBPJ) to restore the polarization imbalance of M/M2 macrophages in EAU rats. In addition, miR-223-3p could also inhibit NLRP3 inflammasome activation and inflammasome-induced pyroptosis in ocular tissues. Taken together, our findings indicate that miR-223-3p serves as an important regulator in M1 macrophage polarization and pyroptosis, thereby alleviating the inflammatory response in uveitis.
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
PDF的下载单位、IP信息已删除 (2025-6-4)

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
圆锥香蕉给ZEcholy的求助进行了留言
1秒前
jisujun发布了新的文献求助10
1秒前
李小宁发布了新的文献求助10
1秒前
4秒前
Stroeve发布了新的文献求助10
5秒前
欧阳月空完成签到,获得积分10
5秒前
5秒前
星辰大海应助李小宁采纳,获得10
6秒前
段一帆发布了新的文献求助10
6秒前
冷艳的姿发布了新的文献求助10
6秒前
7秒前
FIN应助小小采纳,获得30
7秒前
领导范儿应助su采纳,获得10
8秒前
Candy发布了新的文献求助10
8秒前
Rondab应助xiaosu采纳,获得10
9秒前
CodeCraft应助LJJ采纳,获得10
10秒前
10秒前
SYLH应助科研通管家采纳,获得20
11秒前
所所应助科研通管家采纳,获得10
11秒前
科研通AI5应助科研通管家采纳,获得10
11秒前
张金蝶完成签到,获得积分10
11秒前
搜集达人应助科研通管家采纳,获得10
12秒前
CAOHOU应助科研通管家采纳,获得10
12秒前
丘比特应助科研通管家采纳,获得10
12秒前
CAOHOU应助科研通管家采纳,获得10
12秒前
赘婿应助科研通管家采纳,获得10
12秒前
量子星尘发布了新的文献求助30
12秒前
SYLH应助科研通管家采纳,获得20
12秒前
12秒前
12秒前
12秒前
CAOHOU应助科研通管家采纳,获得10
12秒前
Lyuhng+1完成签到 ,获得积分10
13秒前
大个应助十九岁的时差采纳,获得10
14秒前
17秒前
桃花落完成签到,获得积分10
20秒前
su发布了新的文献求助10
20秒前
思源应助汪汪采纳,获得10
20秒前
高兴的天蓝完成签到 ,获得积分10
21秒前
21秒前
高分求助中
A new approach to the extrapolation of accelerated life test data 1000
ACSM’s Guidelines for Exercise Testing and Prescription, 12th edition 500
‘Unruly’ Children: Historical Fieldnotes and Learning Morality in a Taiwan Village (New Departures in Anthropology) 400
Indomethacinのヒトにおける経皮吸収 400
Phylogenetic study of the order Polydesmida (Myriapoda: Diplopoda) 370
基于可调谐半导体激光吸收光谱技术泄漏气体检测系统的研究 350
Robot-supported joining of reinforcement textiles with one-sided sewing heads 320
热门求助领域 (近24小时)
化学 材料科学 医学 生物 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 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 3989334
求助须知:如何正确求助?哪些是违规求助? 3531428
关于积分的说明 11253936
捐赠科研通 3270119
什么是DOI,文献DOI怎么找? 1804887
邀请新用户注册赠送积分活动 882087
科研通“疑难数据库(出版商)”最低求助积分说明 809173