Advances in clinical and experimental medicine : official organ Wroclaw Medical University · 2020
MicroRNA-24 inhibits CDX1 expression in decidual tissues of recurrent spontaneous abortion mice to reduce the abortion risk.
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.
Wang Shuyan, Guo Shishan, Hou Xiaoyan
Аннотация
BACKGROUND: Recurrent spontaneous abortion (RSA), presenting as one of the difficult clinical diseases, has a high incidence rate among women of reproductive age, with a rising trend in recent years.
OBJECTIVES: To confirm a target relationship between miR-24 and CDX1. This study aimed to explore miR-24 expression in decidual tissue under recurrent spontaneous abortion (RSA) and its mechanism of regulating downstream gene CDX1.
MATERIAL AND METHODS: Female CBA/J mice were mated with male BALB/C mice to establish normal pregnancy models, and mated with male DBA/2 mice to establish RSA models. Recurrent spontaneous abortion model mice were randomized into 5 groups: a model group, a NC group, a miR-24 mimic group, a CDX1 vector group, and a miR-24 mimic+CDX1 vector group. Expressions of miR-24, CDX1, VEGF, cleaved caspase-3, Fas, and FasL, as well as apoptosis in decidual tissues, embryonic development and embryo loss rate were compared.
RESULTS: Compared with the normal group, the embryo loss rate, apoptosis rate, and the expressions of cleaved caspase-3, Fas and CDX1 in decidual tissue in other groups were significantly increased, and the expressions of miR-24, VEGF, and FasL were significantly decreased (all p < 0.05). The miR-24 mimic group showed the opposite changes when compared with the model group (all p < 0.05). However, CDX1 overexpression can significantly block the protective effect of miR-24 overexpression on embryonic development (p < 0.05).
CONCLUSIONS: MiR-24 can inhibit CDX1 expression in decidual tissue of RSA mice, thus improving the embryonic development of the mice and reducing the RSA risk.
OBJECTIVES: To confirm a target relationship between miR-24 and CDX1. This study aimed to explore miR-24 expression in decidual tissue under recurrent spontaneous abortion (RSA) and its mechanism of regulating downstream gene CDX1.
MATERIAL AND METHODS: Female CBA/J mice were mated with male BALB/C mice to establish normal pregnancy models, and mated with male DBA/2 mice to establish RSA models. Recurrent spontaneous abortion model mice were randomized into 5 groups: a model group, a NC group, a miR-24 mimic group, a CDX1 vector group, and a miR-24 mimic+CDX1 vector group. Expressions of miR-24, CDX1, VEGF, cleaved caspase-3, Fas, and FasL, as well as apoptosis in decidual tissues, embryonic development and embryo loss rate were compared.
RESULTS: Compared with the normal group, the embryo loss rate, apoptosis rate, and the expressions of cleaved caspase-3, Fas and CDX1 in decidual tissue in other groups were significantly increased, and the expressions of miR-24, VEGF, and FasL were significantly decreased (all p < 0.05). The miR-24 mimic group showed the opposite changes when compared with the model group (all p < 0.05). However, CDX1 overexpression can significantly block the protective effect of miR-24 overexpression on embryonic development (p < 0.05).
CONCLUSIONS: MiR-24 can inhibit CDX1 expression in decidual tissue of RSA mice, thus improving the embryonic development of the mice and reducing the RSA risk.