清晨好,您是今天最早来到科研通的研友!由于当前在线用户较少,发布求助请尽量完整地填写文献信息,科研通机器人24小时在线,伴您科研之路漫漫前行!

Bone Marrow Mesenchymal Stem Cell-Derived Exosomes microRNA-31-5p Repress Pulmonary Fibrosis via IGFBP7.

间充质干细胞 微泡 小RNA 骨髓 干细胞 癌症研究 医学 肺纤维化 生物 细胞生物学 病理 纤维化 遗传学 基因
作者
Lingrui Zhang,Ke Qiu,Chenchen Zhang,Jiaqing Wu
出处
期刊:PubMed
标识
DOI:10.1177/10430342251366273
摘要

Bone marrow mesenchymal stem cell-derived exosomes (BMSCs-Exos) with their molecular cargo have therapeutic potential for pulmonary fibrosis (PF). This research was performed to uncover how microRNA-31-5p (miR-31-5p), carried by BMSCs-Exos, affects PF via modulating IGFBP7. C57BL/6 mice were treated with bleomycin (BLM) to induce PF. Pulmonary function was tested, and fibrotic changes in the mouse lung tissues were examined. Levels of fibrosis-related inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6, were tested. Mouse BMSCs were isolated and identified, and BMSCs-Exos were obtained by ultracentrifugation. Exosome morphology was observed by transmission electron microscopy, the surface markers were measured, and the expression levels of BMSCs-Exo marker proteins were assessed. The targeting relation between miR-31-5p and IGFBP7 was assessed, and the expression of both was tested. After modeling, mice exhibited decreased functional residual capacity, lung compliance, inspiratory capacity, vital capacity, total lung capacity, and forced vital capacity. After 14 days of BLM induction, thickening of the main tracheal wall, fibroblast accumulation, immune cell infiltration in lung interstitium, and increased collagen deposition were observed. Elevated levels of TNF-α, IL-1β, and IL-6 were also noted. BMSCs-Exos attenuated BLM-induced PF, and BMSCs-Exo-derived miR-31-5p ameliorated PF in mice. miR-31-5p was shown to target IGFBP7, diminishing both transcript and protein levels. IGFBP7 overexpression reversed the ameliorative impact of miR-31-5p on PF in mice. BMSCs-Exos ameliorate PF development by delivering miR-31-5p to repress IGFBP7.

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
稻子完成签到 ,获得积分10
5秒前
42秒前
Owen应助zzcc采纳,获得10
42秒前
顺颂时祺发布了新的文献求助10
47秒前
Cumin完成签到 ,获得积分10
47秒前
FashionBoy应助踏实的12采纳,获得10
50秒前
方白秋完成签到,获得积分10
1分钟前
Yafeiyy___完成签到,获得积分10
2分钟前
谭平完成签到 ,获得积分10
2分钟前
小小二完成签到,获得积分10
2分钟前
AiQi完成签到 ,获得积分10
2分钟前
科研通AI2S应助科研通管家采纳,获得10
2分钟前
大医仁心完成签到 ,获得积分10
3分钟前
3分钟前
3分钟前
细心帽子发布了新的文献求助10
3分钟前
UPUP0707发布了新的文献求助10
3分钟前
我是老大应助UPUP0707采纳,获得10
3分钟前
换乘点应助细心帽子采纳,获得10
4分钟前
完美世界应助学业繁忙采纳,获得30
5分钟前
斯文败类应助虚幻心锁采纳,获得10
5分钟前
5分钟前
5分钟前
虚幻心锁完成签到,获得积分10
5分钟前
虚幻心锁发布了新的文献求助10
5分钟前
小小发布了新的文献求助10
5分钟前
小小完成签到,获得积分10
5分钟前
Alisha完成签到,获得积分10
6分钟前
miyamoto应助明理代荷采纳,获得30
6分钟前
6分钟前
踏实的12发布了新的文献求助10
6分钟前
arsenal完成签到 ,获得积分10
8分钟前
8分钟前
zzcc发布了新的文献求助10
8分钟前
zzcc完成签到,获得积分10
9分钟前
dovejingling完成签到,获得积分10
9分钟前
hunajx完成签到,获得积分10
10分钟前
科研通AI2S应助科研通管家采纳,获得10
10分钟前
Wells应助科研通管家采纳,获得10
10分钟前
11分钟前
高分求助中
(应助此贴封号)【重要!!请各位详细阅读】【科研通的精品贴汇总】 10000
F-35B V2.0 How to build Kitty Hawk's F-35B Version 2.0 Model 2000
줄기세포 생물학 1000
Biodegradable Embolic Microspheres Market Insights 888
Quantum reference frames : from quantum information to spacetime 888
The Netter Collection of Medical Illustrations: Digestive System, Volume 9, Part III - Liver, Biliary Tract, and Pancreas (3rd Edition) 600
INQUIRY-BASED PEDAGOGY TO SUPPORT STEM LEARNING AND 21ST CENTURY SKILLS: PREPARING NEW TEACHERS TO IMPLEMENT PROJECT AND PROBLEM-BASED LEARNING 500
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 4471384
求助须知:如何正确求助?哪些是违规求助? 3931180
关于积分的说明 12196419
捐赠科研通 3585335
什么是DOI,文献DOI怎么找? 1970829
邀请新用户注册赠送积分活动 1008788
科研通“疑难数据库(出版商)”最低求助积分说明 902655