Key result
Coxsackie B3 virus infection significantly dysregulated lncRNA expression in the heart, identifying 88 commonly dysregulated lncRNAs across four myocarditis models and 923 fulminant myocarditis-specific lncRNAs.
Why the study?
The roles of long non-coding RNAs in acute myocarditis, particularly fulminant myocarditis, remain unclear.
Specific lncRNAs are significantly dysregulated in CVB3-induced acute and fulminant myocarditis in mice, correlating with cardiac inflammation and dysfunction.
Answers are grounded in this paper and cite their sources.
LncRNA patterns in CVB3 mouse models should not alter clinical practice; leaves open their biomarker or therapeutic roles in human fulminant myocarditis.
Aims: Long non-coding RNAs (lncRNAs) are critical regulators of viral infection and inflammatory responses. However, the roles of lncRNAs in acute myocarditis (AM), especially fulminant myocarditis (FM), remain unclear. Methods: FM and non-fulminant myocarditis (NFM) were induced by coxsackie B3 virus (CVB3) in different mouse strains. Then, the expression profiles of the lncRNAs in the heart tissues were detected by sequencing. Finally, the patterns were analyzed by Pearson/Spearman rank correlation, Kyoto Encyclopedia of Genes and Genomes, and Cytoscape 3.7. Results: First, 1,216, 983, 1,606, and 2,459 differentially expressed lncRNAs were identified in CVB3-treated A/J, C57BL/6, BALB/c, and C3H mice with myocarditis, respectively. Among them, 88 lncRNAs were commonly dysregulated in all four models. Quantitative real-time polymerase chain reaction analyses further confirmed that four out of the top six commonly dysregulated lncRNAs were upregulated in all four models. Moreover, the levels of ENSMUST00000188819, ENSMUST00000199139, and ENSMUST00000222401 were significantly elevated in the heart and spleen and correlated with the severity of cardiac inflammatory infiltration. Meanwhile, 923 FM-specific dysregulated lncRNAs were detected, among which the levels of MSTRG.26098.49, MSTRG.31307.11, MSTRG.31357.2, and MSTRG.32881.28 were highly correlated with LVEF. Conclusion: Expression of lncRNAs is significantly dysregulated in acute myocarditis, which may play different roles in the progression of AM.
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Nie et al. (2021) studied Acute myocarditis (n=100). Coxsackie B3 virus (CVB3) vs. Phosphate-buffered saline (PBS) was evaluated on Differentially expressed lncRNAs in heart tissues (p=<0.05). Coxsackie B3 virus infection significantly dysregulated lncRNA expression in the heart, identifying 88 commonly dysregulated lncRNAs across four myocarditis models and 923 fulminant myocarditis-specific lncRNAs.
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