MicroRNAs (miRNAs) play a key role in various pathological processes like atrial fibrillation (AF), which is a common cardiac arrhythmia. Exosomes are essential information carrier in the intercellular communication. Therefore, this study aimed to investigate the effects of exosomal miR-320d on cardiomyocytes with AF and related mechanisms. To do this, AMSCs were transfected with miR-320d mimics, AMSCs-derived exosomes were co-cultured with cardiomyocytes with AF. MTT, TUNEL staining, flow cytometry, real-time PCR, western blots, and luciferase reporter assays were performed. The results revealed that miR-320d expression was decreased in AF cardiomyocytes. AF increased apoptosis and reduced cell viability in cardiomyocytes. By transfection with miR-320d mimics, the miR-320d level was increased in AMSCs, exosomes and cardiomyocytes, which reversed the effect of AF on cardiomyocytes. STAT3 was down-regulated in AF cardiomyocytes and was a direct target gene of miR-320d. Inhibition of STAT3 abolished the effect of modified exosomes in cardiomyocytes, causing decreased apoptosis and increased cell viability. Taken together, the results suggested that exosomal miR-320d was associated with AF cardiomyocytes apoptosis and cell viability and that the effect of miR-320d on cardiomyocytes is STAT3-dependent. Therefore, this study provides a novel understanding of the molecular basis of AF and provides insight into therapeutic strategies for AF.

中文翻译：

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源自脂肪组织来源的 MSCs 的外泌体 miR-320d 抑制心房颤动 (AF) 心肌细胞的凋亡。

MicroRNAs (miRNAs) 在各种病理过程中发挥关键作用，例如心房颤动 (AF)，这是一种常见的心律失常。外泌体是细胞间通讯中必不可少的信息载体。因此，本研究旨在探讨外泌体 miR-320d 对 AF 心肌细胞的影响及相关机制。为此，用 miR-320d 模拟物转染 AMSCs，将 AMSCs 衍生的外泌体与 AF 心肌细胞共培养。进行了 MTT、TUNEL 染色、流式细胞术、实时 PCR、蛋白质印迹和荧光素酶报告基因测定。结果显示 AF 心肌细胞中 miR-320d 的表达降低。AF 增加了心肌细胞的凋亡并降低了细胞活力。通过转染 miR-320d 模拟物，miR-320d 水平在 AMSCs、外泌体和心肌细胞中增加，这逆转了 AF 对心肌细胞的影响。STAT3 在 AF 心肌细胞中下调，是 miR-320d 的直接靶基因。抑制 STAT3 消除了修饰的外泌体在心肌细胞中的作用，导致细胞凋亡减少和细胞活力增加。总之，结果表明外泌体 miR-320d 与 AF 心肌细胞凋亡和细胞活力相关，并且 miR-320d 对心肌细胞的影响是 STAT3 依赖性的。因此，本研究提供了对 AF 分子基础的新认识，并提供了对 AF 治疗策略的见解。导致细胞凋亡减少和细胞活力增加。总之，结果表明外泌体 miR-320d 与 AF 心肌细胞凋亡和细胞活力相关，并且 miR-320d 对心肌细胞的影响是 STAT3 依赖性的。因此，本研究提供了对 AF 分子基础的新认识，并提供了对 AF 治疗策略的见解。导致细胞凋亡减少和细胞活力增加。总之，结果表明外泌体 miR-320d 与 AF 心肌细胞凋亡和细胞活力相关，并且 miR-320d 对心肌细胞的影响是 STAT3 依赖性的。因此，本研究提供了对 AF 分子基础的新认识，并提供了对 AF 治疗策略的见解。