Abstract
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. 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. 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. 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). 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.
Highlights
Recurrent spontaneous abortion (RSA) is defined as 3 consecutive pregnancy losses in a woman of reproductive age in the setting of 1 identical sexual partner.[1,2] Recurrent spontaneous abortion, presenting as a difficult clinical disease, has a high incidence rate among women of reproductive age, with a rising trend in recent years.[3,4] Exploration on the mechanism of RSA can enrich the theoretical basis in clinical treatment and may provide new critical ideas for RSA treatment.We found that caudal-type homeobox 1 (CDX1) was significantly overexpressed in RSA through preliminary experiments
This study aimed to explore miR-24 expression in decidual tissue under recurrent spontaneous abortion (RSA) and its mechanism of regulating downstream gene CDX1
One research study showed that the expression of enhancer of zeste homologue 2 (EZH2) was significantly downregulated in RSA, and 1 other research study through chromatin immunoprecipitation assay confirmed that EZH2 was obviously bound with CDX1, and through dual-luciferase reporter gene assay verified that EZH2 could negatively regulate CDX1 expression.[5,6]
Summary
Recurrent spontaneous abortion (RSA) is defined as 3 consecutive pregnancy losses in a woman of reproductive age in the setting of 1 identical sexual partner.[1,2] Recurrent spontaneous abortion, presenting as a difficult clinical disease, has a high incidence rate among women of reproductive age, with a rising trend in recent years.[3,4] Exploration on the mechanism of RSA can enrich the theoretical basis in clinical treatment and may provide new critical ideas for RSA treatment.We found that caudal-type homeobox 1 (CDX1) was significantly overexpressed in RSA through preliminary experiments. Recurrent spontaneous abortion, presenting as a difficult clinical disease, has a high incidence rate among women of reproductive age, with a rising trend in recent years.[3,4]. No research at present has confirmed the mechanism of CDX1 affecting RSA. We speculated that CDX1 may be a crucial target in RSA. Many studies have reported microRNA expression regulation in RSA.[7–11]. MiR-24 regulates posttranscriptional expressions mainly by targeting downstream genes. MiR-24 may serve as an important regulatory factor affecting RSA. We further speculated that miR-24 may highly possibly serve as the upstream regulatory component of CDX1 in RSA. 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
Published Version
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