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
Lucas应助程院采纳,获得10
刚刚
刚刚
薯愿完成签到,获得积分10
1秒前
不回首发布了新的文献求助10
1秒前
1秒前
zwj发布了新的文献求助10
1秒前
2秒前
懒猫发布了新的文献求助10
2秒前
2秒前
吴世宇发布了新的文献求助10
3秒前
3秒前
淞33发布了新的文献求助10
3秒前
无花果应助感动的寒风采纳,获得10
4秒前
酷波er应助姚芭蕉采纳,获得10
4秒前
跳跃雨寒完成签到 ,获得积分10
5秒前
慕青应助Ava采纳,获得10
5秒前
6秒前
英俊的铭应助sandra采纳,获得10
6秒前
不配.应助加载文献别卡了采纳,获得20
6秒前
云_123完成签到,获得积分10
6秒前
调研昵称发布了新的文献求助10
6秒前
CipherSage应助王彤彤采纳,获得10
7秒前
FashionBoy应助清森采纳,获得10
8秒前
euphoria发布了新的文献求助10
8秒前
8秒前
wanci应助现实的行云采纳,获得10
9秒前
淞33完成签到,获得积分10
10秒前
10秒前
10秒前
HuanChen应助风清云淡采纳,获得10
10秒前
bkagyin应助叶楠采纳,获得10
11秒前
春风柳上原完成签到 ,获得积分10
11秒前
搜集达人应助Zhouzhou采纳,获得10
12秒前
ZDY完成签到,获得积分10
12秒前
Rank完成签到,获得积分10
12秒前
12秒前
BOOK思议发布了新的文献求助10
13秒前
懒猫完成签到,获得积分10
14秒前
可以的发布了新的文献求助10
14秒前
15秒前
高分求助中
Evolution 3rd edition 1500
保险藏宝图 1000
Lire en communiste 1000
Mantiden: Faszinierende Lauerjäger Faszinierende Lauerjäger 700
PraxisRatgeber: Mantiden: Faszinierende Lauerjäger 700
A new species of Coccus (Homoptera: Coccoidea) from Malawi 500
2-Acetyl-1-pyrroline: an important aroma component of cooked rice 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 3181497
求助须知:如何正确求助?哪些是违规求助? 2831768
关于积分的说明 7986447
捐赠科研通 2493734
什么是DOI,文献DOI怎么找? 1330309
科研通“疑难数据库(出版商)”最低求助积分说明 635955
版权声明 602955