Long non-coding RNA (lncRNA) has been associated with human diseases. To study the role of lncRNA in the pathogenic mechanism of acute fulminant myocarditis (AFM), we used a microarray to analyze lncRNA and messenger RNA (mRNA) expression in leukocyte samples from AFM patients and normal children. In total, using a 2/0.5-fold change and P < 0.05 as the cutoff criteria, we found that 3,101 lncRNAs and 2,170 mRNAs were differentially expressed in AFM patients. Quantitative real-time polymerase chain reaction (RT-qPCR) analysis was used to verify the microarray data. Eight differentially expressed molecules were randomly selected, including 3 upregulated lncRNAs, 3 downregulated lncRNAs, and 2 upregulated mRNAs. Among them, 7 expression profiles were consistent with the microarray results. Gene Ontology enrichment and Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis were used to investigate the biological functions of these genes. Establishment of a lncRNA-mRNA co-expression network and lncRNA target predication were performed to study the molecular interactions of these molecules. Our study is the first to use microarrays to examine the lncRNA and mRNA expression profiles associated with AFM, and the results indicate that the immune system plays an important role in AFM. These findings may provide a new perspective for the pathogenesis, diagnosis, and therapy of AFM.
Aim: To assess differential expression profiles of circular RNAs (circRNAs) and explore their possible functions in children with fulminant myocarditis. Materials & methods: circRNA microarray experiments were carried out for determining differential expression profiles of circRNAs in three children with fulminant myocarditis and three healthy volunteers. Functional analysis and circRNA–miRNA–mRNA interaction network building were conducted to study biological functions. Results: This work identified 2281 upregulated and 892 downregulated circRNAs. Further assessment confirmed hsa_circ_0071542 upregulation (2.5-fold) in fulminant myocarditis. Functional analysis demonstrated the differentially expressed circRNAs mainly contributed to inflammation and immunity. Conclusion: circRNAs might have substantial roles in pediatric fulminant myocarditis, and hsa_circ_0071542 could serve as a promising biomarker.
Although selection of the early age at puberty in gilts will make for a favorable effect on the reproductivity of sow, a large proportion of phenotypic variation in age at puberty of gilts cannot be explained by genetics. Previous studies have implicated hypothalamic DNA methylation in the onset of puberty in mammals. However, the underlying molecular mechanism regarding the regulation of the onset of puberty has remained largely unexplored in gilts. Herein, the genome-scale DNA methylation of hypothalamus was acquired, using the reduced representation bisulfite sequencing, to compare and describe the changes of DNA methylation across Pre-, In- and Post-pubertal gilts. In this study, the average methylation levels of CpGs and CpHs (where H = C, T, or A) in CpG islands- and gene-related regions were gradually decreased in hypothalamic methylomes during the pubertal transition. Comparisons of Pre- vs. In-, In- vs. Post-, and Pre- vs. Post-pubertal stage revealed that there were 85726, 92914, and 100421 differentially methylated CpGs and 5940, 14804, and 16893 differentially methylated CpHs (where H = C, T, or A) in the hypothalamic methylomes. The methylation changes of CpHs were more dynamic than that of CpGs, and methylation changes of CpGs and CpHs were likely to be, respectively, involved in the developmental processes of reproduction and the molecular processes of cellular communications in the hypothalamus. Moreover, methylation changes of CpHs were observed to overrepresent in the quantitative trait loci of age at puberty, and the biological function of these CpH methylation changes was enriched in the pancreas development in gilts. Furthermore, the mRNA levels of several differentially CpG or CpH methylated genes related to the transcription of RNA II polymerase, GnRH signaling pathway, Estrogen signaling pathway, PI3K-AKt signaling pathway, and Insulin signaling pathway, including MAX, MMP2, FGF11, IGF1R, FGF21, and GSK3B, were significantly changed across these pubertal stages in the hypothalamus. These results will help our understanding of how DNA methylation contributes to phenotypic variation of age at puberty.
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