International journal of cardiology · 2016
MicroRNA-98 plays a critical role in experimental myocarditis.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Chen Xiao, Dong Shuo, Zhang Ningning, Chen Liang, Li Mao-Gang, Yang Ping-Chang, Song Jiangping
Аннотация
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.
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.