Exosomal CircHIPK3 Released from Hypoxia-Induced Cardiomyocytes Regulates Cardiac Angiogenesis after Myocardial Infarction
Joint Authors
Zhao, Ranzun
Shi, Bei
Wang, Yan
Liu, Weiwei
Wang, Zhenglong
Shen, Changyin
Yuan, Jinson
Li, Chaofu
Deng, Wenwen
Zhang, Wei
Ge, Junbo
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-19, 19 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-07-14
Country of Publication
Egypt
No. of Pages
19
Main Subjects
Abstract EN
Exosomes play critical roles in mediating cell-to-cell communication by delivering noncoding RNAs (including miRNAs, lncRNAs, and circRNAs).
Our previous study found that cardiomyocytes (CMs) subjected to hypoxia released circHIPK3-rich exosomes to regulate oxidative stress damage in cardiac endothelial cells.
However, the role of exosomes in regulating angiogenesis after myocardial infarction (MI) remains unknown.
The aim of this study was to establish the effects of exosomes derived from hypoxia-induced CMs on the migration and angiogenic tube formation of cardiac endothelial cells.
Here, we reported that hypoxic exosomes (HPC-exos) can effectively reduce the infarct area and promote angiogenesis in the border surrounding the infarcted area.
HPC-exos can also promote cardiac endothelial cell migration, proliferation, and tube formation in vitro.
However, these effects were weakened after silencing circHIPK3 in hypoxia-induced CMs.
We further verified that silencing and overexpressing circHIPK3 changed cardiac endothelial cell proliferation, migration, and tube formation in vitro by regulating the miR-29a expression.
In addition, exosomal circHIPK3 derived from hypoxia-induced CMs first led to increased VEGFA expression by inhibiting miR-29a activity and then promoted accelerated cell cycle progression and proliferation in cardiac endothelial cells.
Overexpression of miR-29a mimicked the effect of silencing circHIPK3 on cardiac endothelial cell activity in vitro.
Thus, our study provides a novel mechanism by which exosomal circRNAs are involved in the communication between CMs and cardiac endothelial cells.
American Psychological Association (APA)
Wang, Yan& Zhao, Ranzun& Shen, Changyin& Liu, Weiwei& Yuan, Jinson& Li, Chaofu…[et al.]. 2020. Exosomal CircHIPK3 Released from Hypoxia-Induced Cardiomyocytes Regulates Cardiac Angiogenesis after Myocardial Infarction. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-19.
https://search.emarefa.net/detail/BIM-1205608
Modern Language Association (MLA)
Wang, Yan…[et al.]. Exosomal CircHIPK3 Released from Hypoxia-Induced Cardiomyocytes Regulates Cardiac Angiogenesis after Myocardial Infarction. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-19.
https://search.emarefa.net/detail/BIM-1205608
American Medical Association (AMA)
Wang, Yan& Zhao, Ranzun& Shen, Changyin& Liu, Weiwei& Yuan, Jinson& Li, Chaofu…[et al.]. Exosomal CircHIPK3 Released from Hypoxia-Induced Cardiomyocytes Regulates Cardiac Angiogenesis after Myocardial Infarction. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-19.
https://search.emarefa.net/detail/BIM-1205608
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1205608