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首页> 外文期刊>Animal Genetics >Transcriptome analysis of muscle in horses suffering from recurrent exertional rhabdomyolysis revealed energetic pathway alterations and disruption in the cytosolic calcium regulation.
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Transcriptome analysis of muscle in horses suffering from recurrent exertional rhabdomyolysis revealed energetic pathway alterations and disruption in the cytosolic calcium regulation.

机译:患有反复劳累性横纹肌溶解症的马的肌肉转录组分析显示能量途径改变和胞浆钙调节的破坏。

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Recurrent exertional rhabdomyolysis (RER) is frequently observed in race horses like trotters. Some predisposing genetic factors have been described in epidemiological studies. However, the exact aetiology is still unknown. A calcium homeostasis disruption was suspected in previous experimental studies, and we suggested that a transcriptome analysis of RER muscles would be a possible way to investigate the pathway disorder. The purpose of this study was to compare the gene expression profile of RER vs. control muscles in the French Trotter to determine any metabolic or structural disruption. Total RNA was extracted from the gluteal medius and longissimus lumborum muscles after biopsies in 15 French Trotter horses, including 10 controls and 5 RER horses affected by 'tying-up' with high plasmatic muscular enzyme activities. Gene expression analysis was performed on the muscle biopsies using a 25K oligonucleotide microarray, which consisted of 24009 mouse and 384 horse probes. Transcriptome analysis revealed 191 genes significantly modulated in RER vs. control muscles (P<0.05). Many genes involved in fatty acid oxidation (CD36/FAT, SLC25A17), the Krebs cycle (SLC25A11, SLC25A12, MDH2) and the mitochondrial respiratory chain were severely down-regulated (tRNA, MT-ND5, MT-ND6, MT-COX1). According to the down-regulation of RYR1, SLC8A1 and UCP2 and up-regulation of APP and HSPA5, the muscle fibre calcium homeostasis seemed to be greatly affected by an increased cytosolic calcium and a depletion of the sarcoplasmic reticulum calcium. Gene expression analysis suggested an alteration of ATP synthesis, with severe mitochondrial dysfunction that could explain the disruption of cytosolic calcium homeostasis and inhibition of muscular relaxation.
机译:经常出现劳累性横纹肌溶解症(RER),在诸如小跑的赛马中。流行病学研究已经描述了一些易感遗传因素。但是,确切的病因仍然未知。在先前的实验研究中怀疑存在钙稳态平衡破坏,我们建议对RER肌肉进行转录组分析可能是研究该途径障碍的一种可能方法。这项研究的目的是比较法式猪蹄RER与对照肌肉的基因表达谱,以确定任何代谢或结构破坏。在对15例法国Trotter马进行活检后,从臀中肌和腰最长肌提取总RNA,其中包括10例对照和5例RER马,这些马受“绑扎”并具有高血浆肌酶活性。使用25K寡核苷酸微阵列对肌肉活检样本进行基因表达分析,该芯片由24009小鼠和384马探针组成。转录组分析显示,相对于对照肌肉,RER中有191个基因被显着调节( P <0.05)。许多基因参与脂肪酸氧化( CD36 / FAT , SLC25A17 ),克雷布斯循环( SLC25A11 , SLC25A12 , MDH2 )和线粒体呼吸链被严重下调( tRNA , MT-ND5 , MT-ND6 , MT-COX1 )。根据 RYR1 , SLC8A1 和 UCP2 的下调以及 APP 和的上调HSPA5 (肌纤维钙稳态)似乎受到胞浆钙增加和肌浆网钙消耗的影响。基因表达分析表明,ATP合成发生了改变,伴有严重的线粒体功能异常,这可以解释细胞质钙稳态的破坏和肌肉松弛的抑制。

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