• Jianan Li, Qingchun Zhang, and Haimiao Jiao.
• Department of Cardiovascular Surgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, PR China. Electronic address: ahslyylja@163.com.
• J Formos Med Assoc. 2021 Jul 1; 120 (7): 1512-1519.

Background/PurposemiR-23a is a pro-hypertrophic miRNA that inhibits M2 macrophage polarization. A previous study demonstrated that lncRNA NRON alleviated atrial fibrosis through suppression of M1 macrophages activated by atrial myocytes. This study aimed to determine whether NRON promotes M2 macrophage polarization and alleviates atrial fibrosis through suppressing exosomal miR-23a derived from atrial myocytes.MethodsMouse atrial myocytes were transfected with the NRON overexpression vector or empty vector, followed by Ang II treatment. Exosomes were isolated from the treated atrial myocytes and then co-cultured with RAW264.7 macrophages. The culture medium from RAW264.7 macrophages treated as described above was added to mouse atrial fibroblasts for incubation.ResultsWe found that exosomes derived from Ang II-treated atrial myocytes inhibited M2 macrophage polarization by transferring miR-23a. NFATc3 could directly bind to the miR-23a promoter. Overexpression of NRON inhibited the expression of miR-23a by inhibiting NFATc3 nuclear transport in Ang II-treated atrial myocytes, resulting in a decrease in the level of miR-23a in atrial myocyte-derived exosomes. Meanwhile, exosomes derived from NRON-overexpressing atrial myocytes promoted M2 macrophage polarization and inhibited expression of fibrosis markers in atrial fibroblasts.ConclusionNRON promotes M2 macrophage polarization and alleviates atrial fibrosis through suppressing exosomal miR-23a derived from atrial myocytes.Copyright © 2020 Formosan Medical Association. Published by Elsevier B.V. All rights reserved.

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