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
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.
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.
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.