Coxsackieviruses B3 infection of myocardial microvascular endothelial cells activates fractalkine via the ERK1/2 signaling pathway

Wen,Jili; Huang,Congxin

doi:10.3892/mmr.2017.7536

Coxsackieviruses B3 infection of myocardial microvascular endothelial cells activates fractalkine via the ERK1/2 signaling pathway

Authors:
- Jili Wen
- Congxin Huang
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Affiliations: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China
Published online on: September 20, 2017 https://doi.org/10.3892/mmr.2017.7536
Pages: 7548-7552
Copyright: © Wen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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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