Micro RNA-98 plays a critical role in experimental myocarditis

Abstract Background and aims Myocarditis is inflammation in the heart; its pathogenesis is to be further investigated. Activities of micro RNAs (miR) are associated with immune inflammation. This study tests a hypothesis that miR-98 is involved in the development of myocarditis. Methods BALB/c mice...

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Bibliographic Details
Published inInternational journal of cardiology
Main Authors Chen, Xiao, Dong, Shuo, Zhang, Ningning, Chen, Liang, Li, Mao-Gang, Yang, Ping-Chang, Song, Jiangping
Format Journal Article
LanguageEnglish
Published 2016
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Summary:Abstract Background and aims Myocarditis is inflammation in the heart; its pathogenesis is to be further investigated. Activities of micro RNAs (miR) are associated with immune inflammation. This study tests a hypothesis that miR-98 is involved in the development of myocarditis. Methods BALB/c mice were immunized with cardiac α-myosin heavy chain peptides (MyHC-α) to induce myocarditis. The effects of miR-98 on regulation of interleukin (IL)-10 were assessed by real time RT-PCR. Results Mice immunized with MyHC-α showed myocarditis and lower frequency of IL-10+ B cells (B10 cell) in the hearts. Expression of miR-98 was higher, IL-10 was lower, in B cells isolated from the mouse hearts with myocarditis, which was negatively correlated with each other. Exposure to tumor necrosis factor-α up regulated miR-98 expression in B cells. Over-expression of miR-98 suppressed IL-10 expression in B cells. Blocking miR-98 or adoptively transplanting B10 cells attenuated experimental myocarditis. Conclusions miR-98 suppresses IL-10 expression in B cells in the heart, which plays an important role in myocarditis. MiR-98 may be a therapeutic target in the treatment of myocarditis.
ISSN:0167-5273
1874-1754
DOI:10.1016/j.ijcard.2016.11.263