GW28-e0427 MiR-155 in macrophage regulates cardiac function and fibrosis after myocardial infarction possibly through SOCS1-dependent inflammatory response

Methods MiR-155 knockin (miR-155+/+) and knockout (miR-155-/-) mice were obtained by bone marrow transplantation in wild-type (WT) C57BL/6J mice. Conclusions In conclusion, our results suggested that miR-155 accounts for the impairment of cardiac function and ventricular remodeling after MI, and suc...

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Bibliographic Details
Published in:Journal of the American College of Cardiology 2017-10, Vol.70 (16), p.C12-C12
Main Authors: Zhang, Yinfen, He, Wangwei, Huang, Yu, Lu, Yongquan, Zhu, Liyuan, Lin, Lin, Li, Jun, Xie, Qiang
Format: Article
Language:English
Subjects:
Cardiology
Fibrosis
Heart attacks
Heart diseases
Inflammation
Inflammatory response
Macrophages
miRNA
Myocardial infarction
Rodents
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Summary:Methods MiR-155 knockin (miR-155+/+) and knockout (miR-155-/-) mice were obtained by bone marrow transplantation in wild-type (WT) C57BL/6J mice. Conclusions In conclusion, our results suggested that miR-155 accounts for the impairment of cardiac function and ventricular remodeling after MI, and such effects could be associated with SOCS1-mediated inflammatory process.
ISSN:0735-1097
1558-3597
DOI:10.1016/j.jacc.2017.07.043