背景:微小RNA(miRNA)是心脏和肾脏正常发育阶段的重要调节因子。然而,目前尚不清楚miRNA在2型心肾综合征(CRS)中的表达.本研究旨在检测miRNAs的差异表达,阐明差异表达的miRNA靶基因在2型CRS中的主要富集途径。
方法:健康对照组5例(第1组),慢性心力衰竭(CHF,第2组)和7例2型CRS(第3组)纳入,分别。从各组外周血中提取总RNA。预测与2型CRS密切相关的miRNA靶基因和生物信号通路,AgilentmiRNA微阵列平台用于分离的总RNA样品的miRNA谱分析和生物信息学分析.
结果:在进行微阵列分析以筛选三组不同样品中差异表达的循环miRNA后,预测了差异miRNAs的靶基因和生物信息学通路。与组1相比,在组3中发现总共38个差异miRNA(15个上调和23个下调),并且与组2相比,在组3中发现总共42个差异miRNA(11个上调和31个下调)。根据基因本体论(GO)功能和京都基因与基因组百科全书(KEGG)通路分析,分子功能的十大清单,细胞组成和生物过程,并在三组中区分差异表达miRNA的预测基因靶标的前30条信号通路。
结论:在CHF和2型CRS患者之间,miRNA差异表达。预测差异表达miRNAs的靶基因,利用GO功能和KEGG通路分析可能揭示CRS的分子机制。循环miRNA可能有助于CRS的诊断,需要进一步和更大的研究来增强我们研究结果的稳健性。
BACKGROUND: MicroRNAs (miRNAs) are important regulatory factors in the normal developmental stages of the heart and kidney. However, it is currently unclear how miRNA is expressed in type 2 cardiorenal syndrome (CRS). This study aimed to detect the differential expression of miRNAs and to clarify the main enrichment pathways of differentially expressed miRNA target genes in type 2 CRS.
METHODS: Five cases of healthy control (Group 1), eight of chronic heart failure (CHF, Group 2) and seven of type 2 CRS (Group 3) were enrolled, respectively. Total RNA was extracted from the peripheral blood of each group. To predict the miRNA target genes and biological signalling pathways closely related to type 2 CRS, the Agilent miRNA microarray platform was used for miRNA profiling and bioinformatics analysis of the isolated total RNA samples.
RESULTS: After the microarray analysis was done to screen for differentially expressed circulating miRNAs among the three different groups of samples, the target genes and bioinformatic pathways of the differential miRNAs were predicted. A total of 38 differential miRNAs (15 up- and 23 down-regulated) were found in Group 3 compared with Group 1, and a total of 42 differential miRNAs (11 up- and 31 down-regulated) were found in Group 3 compared to Group 2. According to the Gene Ontology (GO) function and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway analysis, the top 10 lists of molecular functions, cellular composition and biological processes, and the top 30 signalling pathways of predicted gene targets of the differentially expressed miRNAs were discriminated among the three groups.
CONCLUSIONS: Between the patients with CHF and type 2 CRS, miRNAs were differentially expressed. Prediction of target genes of differentially expressed miRNAs and the use of GO function and KEGG pathway analysis may reveal the molecular mechanisms of CRS. Circulating miRNAs may contribute to the diagnosis of CRS, and further and larger studies are needed to enhance the robustness of our findings.