Myasthenia gravis (MG) is a disease involving neuromuscular transmission that causes fatigue of skeletal muscles and fluctuating weakness. It has been shown that impairment of myogenic differentiation and myofiber maturation may be the underlying cause of MG. In this study, we detected the abnormal expression of circular RNA (circRNA) using next-generation sequencing in patients with MG. We then investigated the regulatory mechanism and the relationship among circRNA, microRNA, and messenger RNA using quantitative reverse-transcription polymerase chain reaction, bioinformatics analysis, and luciferase report analysis. The expression of inflammatory cytokines and regulatory T lymphocytes was shown to be increased. Circ-FBL was significantly increased in MG patients. Bioinformatics and luciferase report analyses confirmed that miR-133 and PAX7 were the downstream targets of circ-FBL. Overexpression of circ-FBL promoted myoblast proliferation by regulation of miR-133/PAX7. Taken together, our study showed that upregulation of circ-FBL promoted myogenic proliferation in patients with MG by regulating miR-133/PAX7.

中文翻译：

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circ-FBL 的上调通过调节 miR-133/PAX7 促进重症肌无力的肌源性增殖

重症肌无力 (MG) 是一种涉及神经肌肉传递的疾病，会导致骨骼肌疲劳和波动性无力。已经表明，肌原性分化和肌纤维成熟受损可能是 MG 的根本原因。在本研究中，我们使用新一代测序技术检测了 MG 患者中环状 RNA (circRNA) 的异常表达。然后，我们使用定量逆转录聚合酶链反应、生物信息学分析和荧光素酶报告分析研究了 circRNA、microRNA 和信使 RNA 之间的调控机制和关系。显示炎性细胞因子和调节性 T 淋巴细胞的表达增加。MG患者的Circ-FBL显着增加。生物信息学和荧光素酶报告分析证实 miR-133 和 PAX7 是 circ-FBL 的下游靶标。circ-FBL 的过表达通过调节 miR-133/PAX7 促进成肌细胞增殖。总之，我们的研究表明，circ-FBL 的上调通过调节 miR-133/PAX7 促进了 MG 患者的肌源性增殖。