Abstract
Viral myocarditis (VMC) is a common cardiovascular disease, and microRNAs (miRNAs) have been postulated to be involved in its pathology. Using microarrays, we observed that miRNA-21 and -146b were upregulated in a murine model of VMC. We also found that miRNA-451 was downregulated. In vivo silencing of miRNA-21 and -146b resulted in less-severe VMC. Overexpression of miRNA-451 did not ameliorate the severity of VMC. Further work revealed that inhibition of miRNA-21 and -146b decreased the expression levels of Th17 and RORγt . Overexpression of miRNA-451 had no effect on IL-17 and RORγt expression. Inhibition of miRNA-21 and -146b might ameliorate myocardium inflammation by mediating downregulation of RORγt expression, indicating that these miRNAs are involved in the pathogenesis of murine VMC.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Differentiation / drug effects*
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Cell Line
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Coxsackievirus Infections* / genetics
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Coxsackievirus Infections* / physiopathology
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Coxsackievirus Infections* / virology
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Disease Models, Animal
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Enterovirus B, Human / pathogenicity*
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Gene Expression Profiling
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Humans
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Male
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Mice
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Mice, Inbred BALB C
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MicroRNAs / genetics
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MicroRNAs / metabolism
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MicroRNAs / pharmacology*
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Myocarditis* / genetics
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Myocarditis* / physiopathology
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Myocarditis* / virology
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Myocardium / metabolism
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Myocardium / pathology
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Nuclear Receptor Subfamily 1, Group F, Member 3
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Oligonucleotide Array Sequence Analysis
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Th17 Cells / cytology*
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Up-Regulation
Substances
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MIRN146 microRNA, human
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MIRN21 microRNA, human
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MicroRNAs
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Nuclear Receptor Subfamily 1, Group F, Member 3
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Rorc protein, mouse