circRNAs deregulation in exosomes derived from BEAS-2B cells is associated with vascular stiffness induced by PM2.5

竞争性内源性RNA 粘合连接 小RNA 细胞生物学 生物 表型 发病机制 化学 下调和上调 免疫学 基因 钙粘蛋白 细胞 长非编码RNA 生物化学
作者
Qingping Liu,Yaling Zhang,Bin Han,Mengruo Wang,Huaifang Hu,Jie Ning,Wentao Hu,Mei‐Yu Chen,Yaxian Pang,Yuanyuan Chen,Lei Bao,Yujie Niu,Rong Zhang
出处
期刊:Journal of Environmental Sciences-china [Elsevier]
卷期号:137: 527-539 被引量:1
标识
DOI:10.1016/j.jes.2023.02.027
摘要

As an environmental pollutant, ambient fine particulate matter (PM2.5) was linked to cardiovascular diseases. The molecular mechanisms underlying PM2.5-induced extrapulmonary disease has not been elucidated clearly. In this study the ambient PM2.5 exposure mice model we established was to explore adverse effects of vessel and potential mechanisms. Long-term PM2.5 exposure caused reduced lung function and vascular stiffness in mice. And chronic PM2.5 induced migration and epithelial-mesenchymal transition (EMT) phenotype in BEAS-2B cells. After PM2.5 treatment, the circRNAs and mRNAs levels of exosomes released by BEAS-2B cells were detected by competing endogenous RNA (ceRNA) array, which contained 1664 differentially expressed circRNAs (DE-circRNAs) and 308 differentially expressed mRNAs (DE-mRNAs). By bioinformatics analysis on host genes of DE-circRNAs, vascular diseases and some pathways related to vascular diseases including focal adhesion, tight junction and adherens junction were enriched. Then, ceRNA network was constructed, and DE-mRNAs in ceRNA network were conducted functional enrichment analysis by Ingenuity Pathway Analysis, which indicated that hsa_circ_0012627, hsa_circ_0053261 and hsa_circ_0052810 were related to vascular endothelial dysfunction. Furthermore, it was verified experimentally that ExoPM2.5 could induce endothelial dysfunction by increased endothelial permeability and decreased relaxation in vitro. In present study, we investigated in-depth knowledge into the molecule events related to PM2.5 toxicity and pathogenesis of vascular diseases.
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
Ab完成签到,获得积分10
刚刚
orixero应助十二十三采纳,获得10
刚刚
1秒前
筱雪芲完成签到,获得积分10
2秒前
moumou完成签到,获得积分10
2秒前
3秒前
Darknewnew完成签到,获得积分10
3秒前
3秒前
中午发布了新的文献求助10
4秒前
5秒前
shanage应助木头采纳,获得10
6秒前
djbj2022发布了新的文献求助20
6秒前
劲秉应助木头采纳,获得10
6秒前
CodeCraft应助木头采纳,获得10
6秒前
思源应助木头采纳,获得10
6秒前
彭于晏应助木头采纳,获得10
6秒前
完美世界应助木头采纳,获得10
6秒前
JamesPei应助木头采纳,获得10
6秒前
科研通AI2S应助木头采纳,获得10
6秒前
科研通AI2S应助木头采纳,获得10
6秒前
斯文败类应助许win采纳,获得10
6秒前
bull发布了新的文献求助10
7秒前
斯文败类应助Ab采纳,获得30
8秒前
xanthesai发布了新的文献求助10
8秒前
8秒前
不配.应助菅露露采纳,获得20
8秒前
9秒前
NexusExplorer应助电闪采纳,获得10
9秒前
吃吃发布了新的文献求助10
9秒前
13秒前
13秒前
13秒前
葳蕤苍生完成签到,获得积分10
14秒前
Maple完成签到,获得积分10
14秒前
鲲之小完成签到 ,获得积分10
14秒前
15秒前
16秒前
17秒前
18秒前
zhou发布了新的文献求助10
19秒前
高分求助中
Spray / Wall-interaction Modelling by Dimensionless Data Analysis 2000
Evolution 3rd edition 1500
Mantiden: Faszinierende Lauerjäger Faszinierende Lauerjäger 700
PraxisRatgeber: Mantiden: Faszinierende Lauerjäger 700
ALA生合成不全マウスでの糖代謝異常の分子機構解析 520
Mathematics and Finite Element Discretizations of Incompressible Navier—Stokes Flows 500
A new species of Coccus (Homoptera: Coccoidea) from Malawi 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 3187972
求助须知:如何正确求助?哪些是违规求助? 2837589
关于积分的说明 8016293
捐赠科研通 2500276
什么是DOI,文献DOI怎么找? 1334868
科研通“疑难数据库(出版商)”最低求助积分说明 637310
邀请新用户注册赠送积分活动 605364