Ischemia challenged epicardial adipose tissue stem cells-derived extracellular vesicles alter the gene expression of cardiac fibroblasts to cardiomyocyte like phenotype

细胞生物学 脂肪组织 下调和上调 生物 再生医学 干细胞 分子生物学 内分泌学 基因 遗传学
作者
Finosh G. Thankam,Sharona Sedighim,Rebecca Kuan,Devendra K. Agrawal
出处
期刊:Translational Research [Elsevier BV]
卷期号:254: 54-67 被引量:21
标识
DOI:10.1016/j.trsl.2022.10.004
摘要

The present study hypothesizes that the ischemic insults activate epicardial adipose tissue-derived stem cells (EATDS) to secrete extracellular vesicles (EVs) packed with regenerative mediators to alter the gene expression in cardiac fibroblasts (CF). EATDS and CF were isolated from hyperlipidemic microswine and EVs were harvested from control, simulated ischemia (ISC) and ischemia-reperfusion (ISC/R) groups. The in vitro interaction between ISC–EVs and CF resulted in the upregulation of cardiomyocyte-specific transcription factors including GATA4, Nkx2.5, IRX4, and TBX5 in CF and the healing marker αSMA and the downregulation of fibroblast biomarkers such as vimentin, FSP1, and podoplanin and the cardiac biomarkers such as troponin-I and connexin-43. These results suggest a cardiomyocyte-like phenotype as confirmed by immunostaining and Western blot. The LC-MS/MS analysis of ISC–EVs LGALS1, PRDX2, and CCL2 to be the potent protein mediators which are intimately involved in versatile regenerative processes and connected with a diverse array of regenerative genes. Moreover, the LGALS1+, PRDX2+, and CCL2+ EATDS phenotypes were deciphered at single cell resolution revealing corresponding sub-populations with superior healing potential. Overall, the findings unveiled the healing potential of EATDS-derived EVs and sub-populations of regenerative EATDS promising novel translational opportunities in improved cardiac healing following ischemic injury.
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
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
阮婷发布了新的文献求助10
1秒前
开心诗珊完成签到,获得积分10
2秒前
科研hunzi发布了新的文献求助10
2秒前
Fs应助muhong采纳,获得30
3秒前
完美世界应助科研混子采纳,获得10
3秒前
如雨坠完成签到 ,获得积分10
3秒前
yjh123给xinlinwang的求助进行了留言
3秒前
小雪人完成签到,获得积分10
5秒前
Mhj13810完成签到,获得积分10
6秒前
6秒前
Lucas应助卡乐瑞咩吹可采纳,获得10
6秒前
小马甲应助willlow采纳,获得10
10秒前
赘婿应助nature24采纳,获得10
10秒前
Ava应助willlow采纳,获得10
10秒前
10秒前
小二郎应助优雅的豪哥采纳,获得10
10秒前
10秒前
科研通AI6.4应助小雪人采纳,获得10
11秒前
11秒前
科研hunzi完成签到,获得积分10
13秒前
lx应助刘鑫采纳,获得20
13秒前
隐形曼青应助qq采纳,获得10
13秒前
Lucas应助阮婷采纳,获得30
13秒前
迅速静柏应助隐形的凡阳采纳,获得30
15秒前
迅速静柏应助隐形的凡阳采纳,获得30
15秒前
打打应助moonlin采纳,获得10
17秒前
没有昵称完成签到 ,获得积分10
17秒前
lhappy应助南窗下采纳,获得20
17秒前
18秒前
18秒前
zhangnannan发布了新的文献求助10
19秒前
刻苦鼠标发布了新的文献求助10
19秒前
生尽证提发布了新的文献求助10
19秒前
19秒前
20秒前
22秒前
GaCf完成签到 ,获得积分10
22秒前
超帅怜阳发布了新的文献求助10
22秒前
qq完成签到,获得积分10
22秒前
深情安青应助酷酷的语芙采纳,获得30
23秒前
高分求助中
Principles of Economics, 11th Edition 10000
University Physics with Modern Physics, 16th edition 10000
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Arthritis and Related Conditions, An Issue of Orthopedic Clinics 1000
Development of a Bridge Weigh-In-Motion System: A technology to convert the bridge response to the passage of traffic into data on vehicle configurations, speeds, times of travel and weights 1000
ズームレンズの光学設計に関する研究 800
Fundamentals of Pharmaceutical and Biologics Regulations: A Global Perspective, Second Edition 700
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7287447
求助须知:如何正确求助?哪些是违规求助? 8907262
关于积分的说明 18850603
捐赠科研通 6956285
什么是DOI,文献DOI怎么找? 3208552
关于科研通互助平台的介绍 2378495
邀请新用户注册赠送积分活动 2184226