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Coxsackievirus-Induced miR-21 Disrupts Cardiomyocyte Interactions via the Downregulation of Intercalated Disk Components
Coxsackievirus B3 (CVB3) is one of most common causes of heart inflammation and failure. However, the mechanism by which CVB3 induces cardiac damage has not been fully elucidated. Particularly, the involvement of microRNAs (miRNAs), a family of small RNAs controlling the progression of a wide range of diseases, in CVB3 infection is still unclear. These small RNAs are essential to understand the CVB3-caused heart muscle cell injury and have great potential to serve therapeutic purposes. Here, we systematically analyzed the miRNA changes during CVB3 infection and found that miR-21 is increased by viral infection. We further demonstrated that the CVB3-induced miR-21 triggers heart muscle cell damage by interfering with the cell-cell interactions. miR-21 suppresses the levels of components in cell-cell interactions by either promoting the degradation of those proteins or directly inhibiting the protein production. Inhibition of miR-21 can reduce the host injury caused by CVB3 infection. Our findings will shed new lights on the pathogenesis of CVB3-induced heart failure.
Vyšlo v časopise: Coxsackievirus-Induced miR-21 Disrupts Cardiomyocyte Interactions via the Downregulation of Intercalated Disk Components. PLoS Pathog 10(4): e32767. doi:10.1371/journal.ppat.1004070
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004070Souhrn
Coxsackievirus B3 (CVB3) is one of most common causes of heart inflammation and failure. However, the mechanism by which CVB3 induces cardiac damage has not been fully elucidated. Particularly, the involvement of microRNAs (miRNAs), a family of small RNAs controlling the progression of a wide range of diseases, in CVB3 infection is still unclear. These small RNAs are essential to understand the CVB3-caused heart muscle cell injury and have great potential to serve therapeutic purposes. Here, we systematically analyzed the miRNA changes during CVB3 infection and found that miR-21 is increased by viral infection. We further demonstrated that the CVB3-induced miR-21 triggers heart muscle cell damage by interfering with the cell-cell interactions. miR-21 suppresses the levels of components in cell-cell interactions by either promoting the degradation of those proteins or directly inhibiting the protein production. Inhibition of miR-21 can reduce the host injury caused by CVB3 infection. Our findings will shed new lights on the pathogenesis of CVB3-induced heart failure.
Zdroje
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