Timechko Elena E, Severina Marina I, Yakimov Alexey M, Vasilieva Anastasia A, Paramonova Anastasia I, Isaeva Natalya V, Prokopenko Semen V, Dmitrenko Diana V
Russian National Research, V.F. Voyno-Yasenetsky Krasnoyarsk State Medical University, 660022 Krasnoyarsk, Russia.
Krasnoyarsk Regional Clinical Hospital, 3A, Partizana Zheleznyaka str., 660022 Krasnoyarsk, Russia.
Med Sci (Basel). 2025 Aug 8;13(3):118. doi: 10.3390/medsci13030118.
. Myasthenia gravis is an autoimmune neuromuscular disease characterized by fatigue of striated muscles due to impaired neuromuscular transmission. Mitochondrial dysfunction, according to published data, contributes significantly to metabolic abnormalities, oxidative stress and, as a consequence, the persistence of inflammation. MicroRNAs, which are post-transcriptional regulators of expression, are able to contribute to the aberrant functioning of mitochondria. In this study, with the aim of searching for biomarkers at the level of circulating microRNAs and proteins, the expression of three microRNAs was analyzed and the concentration of mitochondrial proteins was measured in the blood plasma of patients with myasthenia gravis ( = 49) in comparison with healthy volunteers ( = 31). . Expression analysis was performed by RT-PCR, mathematical data processing was carried out using the Livak method, and protein concentration was determined by enzyme immunoassay. . Our plasma expression analysis revealed a statistically significant increase in hsa-miR-194-5p expression (Log10 Fold Change = 1.46, -value < 0.0001) and a statistically significant decrease in hsa-miR-148a-3p expression (Log10 Fold Change = -0.65, -value = 0.02). A statistically significant decrease in plasma COQ10A concentration was also found (0.911 [0.439; 1.608] versus 1.815 [1.033; 2.916] for myasthenia gravis and controls, respectively, -value = 0.01). . Our data suggest hsa-miR-148a-3p and hsa-miR-194-5p, as well as COQ10A, as potential biomarkers of mitochondrial dysfunction in myasthenia gravis.
重症肌无力是一种自身免疫性神经肌肉疾病,其特征是由于神经肌肉传递受损导致横纹肌疲劳。根据已发表的数据,线粒体功能障碍在代谢异常、氧化应激以及炎症持续中起重要作用。微小RNA作为转录后表达调节因子,能够导致线粒体功能异常。在本研究中,为了寻找循环微小RNA和蛋白质水平的生物标志物,分析了3种微小RNA的表达,并测量了重症肌无力患者(n = 49)与健康志愿者(n = 31)血浆中线粒体蛋白的浓度。通过RT-PCR进行表达分析,使用Livak方法进行数学数据处理,并通过酶免疫测定法测定蛋白质浓度。我们的血浆表达分析显示,hsa-miR-194-5p表达有统计学意义的增加(Log10倍变化 = 1.46,P值 < 0.0001),hsa-miR-148a-3p表达有统计学意义的降低(Log10倍变化 = -0.65,P值 = 0.02)。还发现血浆中COQ10A浓度有统计学意义的降低(重症肌无力患者和对照组分别为0.911 [0.439; 1.608]和1.815 [1.033; 2.916],P值 = 0.01)。我们的数据表明,hsa-miR-148a-3p、hsa-miR-194-5p以及COQ10A可能是重症肌无力线粒体功能障碍的生物标志物。