Therapeutic Potential of Exosomes Derived From circRNA_0002113 Lacking Mesenchymal Stem Cells in Myocardial Infarction

Tiantian Tian; Feng Li; Ruihua Chen; Zhiwei Wang; Xueming Su; Chao Yang

doi:10.3389/fcell.2021.779524

Therapeutic Potential of Exosomes Derived From circRNA_0002113 Lacking Mesenchymal Stem Cells in Myocardial Infarction

Front Cell Dev Biol. 2022 Jan 19:9:779524. doi: 10.3389/fcell.2021.779524. eCollection 2021.

Authors

Tiantian Tian^{1

2}, Feng Li¹, Ruihua Chen¹, Zhiwei Wang¹, Xueming Su¹, Chao Yang^{1

3}

Affiliations

¹ Hainan Yiling Medical Industry Development Company Ltd., Qionghai, China.
² Center for Biological Science and Technology, Beijing Normal University, Zhuhai, China.
³ State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Taipa, China.

Abstract

Exosomes are participated in the pathogenesis of cardiovascular diseases and can be secreted by mesenchymal stem cells (MSCs). However, the effects of circRNA, delivered by exosomes derived from MSCs, on myocardial injury remain unclear. Hence, this study aims to explore the therapeutic potential of exosomes derived from circRNA_0002113 lacking MSCs in the treatment of myocardial injury in vitro and in vivo. Our results reveal that exosomes derived from circRNA_0002113 lacking MSCs decreased cell apoptosis in anoxia-reoxygenation (A/R) model cells, and reduced myocardial injury by inhibiting nuclear translocation of RUNX1 in vitro and in vivo. Moreover, miR-188-3p, which targets RUNX1 in cardiomyocytes was also found to interact with circRNA_0002113. In conclusion, exosomes derived from circRNA_0002113 lacking MSCs could suppress myocardial infarction by sponging miR-188-3p to regulate RUNX1 nuclear translocation. The circRNA_0002113/miR-188-3p/RUNX1 axis mediated alleviation of apoptosis serves as a novel strategy to treat myocardial I/R injury.

Keywords: MSCs; Runx1; circRNA_0002113; exosomes; miR-188-3p; myocardial infarction.