Journal
INTERNATIONAL JOURNAL OF CARDIOLOGY
Volume 229, Issue -, Pages 75-81Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.ijcard.2016.11.263
Keywords
Heart; Myocarditis; MicroRNA; Interleukin-10; B cells
Categories
Funding
- National Natural Science Foundation of China [81670376]
- PUMC Youth Fund
- CAMS Innovation Fund for Medical Sciences (CIFMS) [2016-I2M-1-015]
- Fundamental Research Funds for the Central Universities
Ask authors/readers for more resources
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 alpha-myosin heavy chain peptides (MyHC-alpha) 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-alpha 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-alpha 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. (c) 2016 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available