高强度间歇游泳运动对有训练大鼠心肌miRNA的差异表达及相关调控通路分析

Differential Expression of Myocardial microRNAs and Analysis of Related Regulatory Pathways in Trained Rats Induced by High-intensity Intermittent Swimming Training

目的:探索有训练大鼠在一次高强度间歇游泳运动后心脏左心室肌中的微小核糖核酸(miRNA)差异表达,从miRNA调控基因表达的视角揭示高强度间歇游泳运动导致心脏功能改变的遗传应答机制。方法:建立大鼠高强度间歇游泳训练(HIST)模型,采用Illumina HiSeq2500测序技术检测各组左心室肌miRNA的表达,对miRNA进行差异表达分析和靶基因预测;对差异表达miRNA靶基因进行GO分析和KEGG通路富集分析。结果:所有样品共鉴定出868个miRNA,其中已知miRNA 531个,新预测miRNA 337个。与对照组相比,间歇组筛选出32个显著差异表达的miRNA,其中22个表达上调,10个表达下调。差异表达miRNA的靶基因涉及心肌细胞的多种生理代谢功能。结论:间歇组大鼠心肌miRNA表达与对照组有显著差异,这些差异表达的miRNA表现出良性与恶性的不同调控趋向,其可能通过靶基因及其编码蛋白调控多种信号通路而实现心脏的重塑,确切机制尚需进一步深入研究。

Objective:To explore the differential expression of left ventricular cardiac muscle miRNA in trained rats after highintensity intermittent swimming training(HIST),and to reveal the genetic response mechanism of cardiac functional changes induced by HIST from the perspective of gene expression regulated by miRNAs.Methods:The HIST rats model was established firstly,and then the expression of left ventricular cardiac muscle miRNA was detected by Illumina HiSeq 2500 sequencing.Differential expression analysis and target genes prediction of miRNA were carried out and gene ontology enrichment analysis and KEGG pathway enrichment analysis were performed for the target genes of differential expression miRNA.Results:868 miRNAs were identified from all samples,of which 531 were known,and 337 were predicted.Compared with control check group,a total of 32 differentially expressed miRNAs were screened out from HIST group,of which 22 miRNAs were up-regulated and 10 were down-regulated.Target genes of differentially expressed miRNAs were associated with a variety of physiological functions of cardiomyocytes.Conclusion:The expression of cardiac muscle miRNA in HIST group was significantly different from that in control check group.These differentially expressed microRNAs showed different regulatory tendencies of benignity and malignancy,which may regulate multiple signaling pathways through target genes and their coding proteins to achieve cardiac remodeling.However,the exact mechanisms need further study.