Myoblast transplantation improves cardiac function after myocardial infarction through attenuating inflammatory responses
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Bo Wang1,*, Likui Zhang2,*, Hao Cao2,*, Junqi Yang1, Manya Wu1, Yali Ma1, Huimin Fan2, Zhenzhen Zhan1 and Zhongmin Liu2
1Key Laboratory of Arrhythmias of the Ministry of Education of China and Institute of Heart Failure, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China
2Department of Cardiac Surgery and Institute of Heart Failure, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China
*These authors contribute equally to this work
Zhenzhen Zhan, email: [email protected]
Zhongmin Liu, email: [email protected]
Keywords: myoblasts, transplantation, myocardial infarction, cardiac function, inflammation
Received: March 10, 2017 Accepted: May 15, 2017 Published: May 27, 2017
Myocardial infarction (MI) is a highly prevalent cardiac emergency, which results in adverse cardiac remodeling and then exacerbates progressive heart failure. Inflammatory responses in cardiac tissue after MI is necessary for myocardium repair and wound healing. However, the excessive inflammation is also a key component of subsequent heart failure pathology. Myoblast transplantation after MI have been fulfilled attractive effects on cardiac repair, but the complications of transplantation and the underlying mechanisms have not been fully elucidated. Here, we found that human myoblast transplantation into minipig myocardium decreased the infiltration of inflammatory cells, the expression levels of many pro-inflammatory genes and the activation of inflammation-related signal pathways, while upregulated the expression levels of anti-inflammatory genes such as IL-10 in cardiac tissue of minipig post-MI, which was contributed to the improved cardiac function, the decreased infarct area and the attenuated myocardial fibrosis. Moreover, co-culture of human myoblasts inhibited the production of IL-1β and TNF-α as well as activation of MAPK and NF-κB signaling pathway induced by damage-associated molecular patterns such as HMGB1 and HSP60 in human THP-1 cells, which was partially attributed to the up-regulated production of IL-10. Collectively, these results indicate that myoblast transplantation ameliorates heart injury and improves cardiac function post-MI through inhibiting the inflammatory response, which provides the novel mechanism for myoblast transplantation therapy of MI.
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