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Stem Cells International
Volume 2017, Article ID 3258035, 9 pages
Research Article

The Optimal Intervention Time of Bone Marrow Mesenchymal Stem Cells in Ameliorating Cardiac Fibrosis Induced by Viral Myocarditis: A Randomized Controlled Trial in Mice

Children’s Heart Center, The Second Affiliated Hospital and Yuying Children’s Hospital, Institute of Cardiovascular Development and Translational Medicine, Wenzhou Medical University, Wenzhou, Zhejiang 325027, China

Correspondence should be addressed to Rongzhou Wu; moc.liamtoh@17zrw

Received 28 April 2017; Revised 30 August 2017; Accepted 11 October 2017; Published 5 December 2017

Academic Editor: Benedetta Bussolati

Copyright © 2017 Tingting Wu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Bone marrow-derived mesenchymal stem cells (BMSCs) have recently been introduced to treat cardiovascular diseases, such as myocardial infarction and dilated cardiomyopathy. Nevertheless, there are few researches focused on the application of BMSCs in treating viral myocarditis, not to mention its optimal intervention timer potential mechanisms. In our study, we concentrated on finding an optimal time window to perform BMSCs treatment in a murine model of myocarditis induced by coxsackievirus B3 (CVB3). On the 1st day, 3rd day, 7th day, and 14th day after BALB/c mice were infected by CVB3, we intravenously injected equivalent BMSCs into the treatment groups. With a 28-day follow-up after inoculation, we found that the ventricular function was significantly improved in the BMSCs treatment group and cardiac fibrosis markedly ameliorated, especially when BMSCs were injected between 1 and 2 weeks after CVB3 inoculation. Furthermore, we demonstrated that after BMSCs treatment, the expressions of TGF-β, col1α1, and col3α1 were significantly decreased. Therefore, we conclude that BMSCs may have a potential to improve CVB3-induced myocarditis by ameliorating cardiac fibrosis through the inhibition of TGF-β expression.