Abstract
Infections by pathogens may lead to cardiovascular diseases, including acute/chronic myocarditis. (Coxsackieviruses B3) CVB3 is considered to be the most common causative agent in m-yocarditis, which can lead to dilated cardiomyopathy. The present study aimed to investigate the mechanism of CVB3-infected myocardial microvascular endothelial cells. The CVB3 infection was detected by 50% tissue culture infective dose (TCID50). The role of fractalkine (FKN) in the infection was detected using western blotting and RNA interference. To assess mitogen-activated protein kinase signaling activity, levels of total and phosphorylated extracellular signal-regulated kinase (ERK)1/2, c-Jun N-terminal kinase, and p38 were measured at 0, 20, 40, and 60 min after CVB3 infection by western blot analysis. The results showed that infection activated FKN via the ERK1/2 signaling pathway. Furthermore, the TCID50 of CVB3 in infected cells was lower compared with that in myocardial microvascular endothelial cells following ERK1/2 inhibition and FKN silencing. CVB3 infection of myocardial microvascular endothelial cells activates FKN via the ERK1/2 signaling pathway. These findings represent a foundation for the development of novel methods of treating CVB3-induced myocarditis.
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