Platelet-derived microRNA-223 attenuates TNF-α induced monocytes adhesion to arterial endothelium by targeting ICAM-1 in Kawasaki disease

血小板 内皮功能障碍 内皮干细胞 血小板活化 医学 单核细胞 内皮 免疫学 内皮细胞活化 内科学
作者
Manli Guo,Shunyang Fan,Qian Chen,Cuiping Jia,Miaoyun Qiu,Yun Bu,Wai Ho Tang,Yuan Zhang
出处
期刊:Frontiers in Immunology [Frontiers Media SA]
卷期号:13
标识
DOI:10.3389/fimmu.2022.922868
摘要

Background Kawasaki disease (KD) is an acute vasculitis that may result in permanent coronary artery damage with unknown etiology. Endothelial cell (EC) dysfunction and platelet hyperactivity are the hallmarks of KD. Platelets are involved in the development of endothelial dysfunction. MiR-223 transferred by platelet microparticles (PMPs) has been found to involve in the functional regulation of endothelial cells in sepsis. However, the role of platelet-derived miR-223 in endothelial dysfunction has not yet been investigated in KD. Objectives We seek to investigate the role of platelet-derived miR-223 in endothelial dysfunction of KD vasculopathy. Methods and results Forty-five acute KD patients and 45 matched controls were randomly recruited in the study. When co-cultured with human coronary artery endothelial cells (HCAECs), KD platelets with higher levels of miR-223 were incorporated into HCAECs, resulting in the horizontal transfer of miR-223. Using KD platelets, PMPs, and platelet-releasate from the same amount of blood co-cultured with HCAECs, we found the increased expression of miR-223 in HCAECs was primarily derived from KD platelets, rather than PMPs or free miRNAs from platelet- releasate. KD platelet-derived miR-223 attenuated TNF-α induced intercellular cell adhesion molecule-1 (ICAM-1) expression in HCAECs. KD platelet-derived miR-223 also suppressed the monocyte adhesion to HCAECs. In vivo , platelet-specific miR-223 knockout (PF4-cre: miR-223 flox/flox ) C57BL/6 mice and miR-223 flox/flox C57BL/6 mice were used. Using Lactobacillus casei cell wall extract (LCWE) to establish KD murine model, we showed that in LCWE-injected PF4-cre: miR-223 flox/flox mice, deficiency of platelet-miR-223 exacerbates the medial thickening of the abdominal aorta, increased ICAM-1 expression with concomitant CD45 + inflammatory cells infiltration into the endothelium compared to LCWE-injected miR-223 flox/flox mice. Conclusions The horizontal transfer of platelet-derived miR-223 suppresses the expression of ICAM-1 in HCAECs, which at least in part attenuates leukocyte adhesion, thereby reducing endothelial damage in KD vasculitis
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
小二郎应助zyf采纳,获得10
刚刚
刚刚
zhw发布了新的文献求助30
刚刚
1秒前
上官若男应助好纠结采纳,获得10
1秒前
北音发布了新的文献求助10
1秒前
小二郎应助sc采纳,获得10
1秒前
2秒前
打打应助TT采纳,获得10
2秒前
3秒前
3秒前
晚风完成签到 ,获得积分10
3秒前
3秒前
3秒前
自由青柏完成签到,获得积分10
5秒前
5秒前
zyr发布了新的文献求助10
5秒前
神光发布了新的文献求助10
5秒前
6秒前
6秒前
6秒前
7秒前
8秒前
NIUBEN发布了新的文献求助10
8秒前
今天爱自己了吗完成签到,获得积分10
8秒前
9秒前
灵巧的翠风完成签到 ,获得积分10
9秒前
9秒前
mayue发布了新的文献求助10
9秒前
其华完成签到 ,获得积分10
10秒前
搜集达人应助fagfagsf采纳,获得10
10秒前
kkkk完成签到,获得积分10
11秒前
小马甲应助活泼冬云采纳,获得10
11秒前
lalala发布了新的文献求助10
12秒前
乐观白桃发布了新的文献求助30
12秒前
12秒前
chan完成签到,获得积分10
12秒前
三岁就爱笑完成签到,获得积分10
13秒前
qwq睡了吗铁柱完成签到,获得积分10
14秒前
Yimi完成签到,获得积分10
14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
Foreign Policy of the French Second Empire: A Bibliography 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 3147464
求助须知:如何正确求助?哪些是违规求助? 2798635
关于积分的说明 7830317
捐赠科研通 2455424
什么是DOI,文献DOI怎么找? 1306789
科研通“疑难数据库(出版商)”最低求助积分说明 627899
版权声明 601587