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Exosomal lncRNA AK139128 Derived from Hypoxic Cardiomyocytes Promotes Apoptosis and Inhibits Cell Proliferation in Cardiac Fibroblasts
Authors Wang L, Zhang J
Received 1 December 2019
Accepted for publication 8 April 2020
Published 12 May 2020 Volume 2020:15 Pages 3363—3376
DOI https://doi.org/10.2147/IJN.S240660
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Linlin Sun
Lei Wang, Jun Zhang
Cardiovascular Department, Cangzhou Central Hospital, Cangzhou, Hebei Province 061001, People’s Republic of China
Correspondence: Jun Zhang Tel +86-13315777566
Email 15245877343@163.com
Introduction: Myocardial infarction (MI) is the leading cause of congestive heart failure and mortality. Hypoxia is an important trigger in the cardiac remodeling of the myocardium in the development and progression of cardiac diseases.
Objective: Thus, we aimed to investigate the effect of hypoxia-induced exosomes on cardiac fibroblasts (CFs) and its related mechanisms.
Materials and Methods: In this study, we successfully isolated and identified the exosomes from hypoxic cardiomyocytes (CMs). Exosomes derived from hypoxic CMs promoted apoptosis and inhibited proliferation, migration, and invasion in CFs. RNA-Seq assay suggested that long noncoding RNA AK139128 (lncRNA AK139128) was found to overexpress in both hypoxic CMs and CMs-secreting exosomes. After coculturing with CFs, hypoxic exosomes increased the expression of AK139128 in recipient CFs. Moreover, exosomal AK139128 derived from hypoxic CMs stimulated CFs apoptosis and inhibited proliferation, migration, and invasion. Furthermore, the effect of exosomal AK139128 derived from hypoxic CMs could also exacerbate MI in the rat model.
Conclusion: Taken together, hypoxia upregulated the level of AK139128 in CMs and exosomes and exosomal AK139128 derived from hypoxic CMs modulated cellular activities of CFs in vitro and in vivo. This study provides a new understanding of the mechanism underlying hypoxia-related cardiac diseases and insight into developing new therapeutic strategies.
Keywords: myocardial infarction, hypoxia, cardiomyocytes, cardiac fibroblasts, exosome, LncRNA AK139128
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