Key result
Upregulation of miR-214 contributes to adverse inflammatory responses during coxsackievirus-induced viral myocarditis by targeting and suppressing the NF-κB signaling suppressor ITCH.
Upregulation of miR-214 exacerbates cardiac inflammation during coxsackievirus infection by targeting the NF-κB suppressor ITCH, highlighting a potential therapeutic target for viral myocarditis.
Viral myocarditis (VM), a severe clinical condition characterized by cardiac inflammation, is most frequently induced as a result of coxsackievirus infection. Evidence suggests that microRNAs may have significant roles in the progression of cardiac injury during coxsackievirus infection. Concurrently, microRNA (miR)-214 was found to be upregulated in the plasma and myocardial cells during this process. In the present study, eight candidate miRNAs, the functions of which are associated with myocarditis, were selected and their expression levels were evaluated by reverse transcription-quantitative polymerase chain reaction. miR-146b and miR-214 were found to have significantly upregulated expression levels in the heart tissues of patients with VM compared with those of the control subjects. Predictions via the use of online bioinformatics tools and confirmed by dual-luciferase assay and western blot analysis, revealed that ITCH, an NF-κB signaling suppressor, was a target gene of miR-214. To investigate the biological function of miR-214, tumor necrosis factor-α and interleukin-6 expression levels were evaluated in HeLa cell culture supernatant. The results revealed that miR-214 overexpression enhanced the expression of the two cytokines. In addition, the function of miR-214 was partially rescued by ITCH overexpression. Subsequently, concurrent results were obtained following experiments in murine cardiac myocytes. In conclusion, the results of the present study demonstrated that miR-214 contributed to the adverse inflammatory response to viral infection of the heart during coxsackievirus infection and is therefore a potential therapeutic target for the treatment of viral myocarditis.
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Chen et al. (2012) studied Viral myocarditis (n=16). miR-214 upregulation vs. Normal expression / Control subjects was evaluated on Expression levels of miR-214 and inflammatory cytokines (p=<0.05). Upregulation of miR-214 contributes to adverse inflammatory responses during coxsackievirus-induced viral myocarditis by targeting and suppressing the NF-κB signaling suppressor ITCH.
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