Meta-analysis of FOXP3 polymorphisms and recurrent spontaneous abortion susceptibility.

BACKGROUND: The polymorphisms of the FOXP3 gene may mediate abnormalities in Tregs, leading to an imbalance in maternal-fetal immune tolerance and ultimately resulting in recurrent spontaneous abortion (RSA). This meta-analysis aims to assess the potential association between FOXP3 polymorphisms and susceptibility to RSA using five specific single nucleotide polymorphisms (SNPs). MATERIALS AND METHODS: By conducting a comprehensive search across databases such as EMBASE, PubMed, Web of Science, Cochrane Library, CNKI, Wanfang, and CBM, we identified suitable studies for inclusion in the meta-analysis. The data extracted from these studies were subjected to analysis using Stata SE 15. To assess the degree of association, we utilized the odds ratio (OR) along with its corresponding 95% confidence intervals (CI). Five specific single nucleotide polymorphisms (SNPs) were employed in assessing the connection between FOXP3 gene polymorphisms and RSA. RESULTS: The meta-analysis demonstrated a significant association between several polymorphisms (rs3761548, rs2232365, rs2232368, rs2280883, and rs2294021) and susceptibility to RSA. Conversely, the FOXP3 rs5902434 polymorphism was not associated with susceptibility to RSA. CONCLUSION: Our meta-analysis suggests that these genetic variations within the FOXP3 gene might play a role in the progression of RSA disease. Meanwhile, large-scale studies that consider multiple factors are needed to validate this finding.

Downregulation of miR-21 is Involved in the Pathogenesis of Infection-Induced Preterm Birth by Targeting NF-κB.

Infection-induced preterm birth (PTB) is contributing to the main factors of increased maternal and fetal morbidity and mortality. Infections and inflammation are often accompanied by histologic chorioamnionitis. Recently, several studies have uncovered that miR-21 and NF-κB are associated with pathological processes of pregnant women. However, the role of miR-21 in infection-induced PTB remains unclear. This study aimed to determine whether miR-21 is involved in the pathogenesis of infection-induced PTB by regulating NF-κB. In this study, we found that the expression of miR-21 was significantly decreased in placental tissues of lipopolysaccharides (LPS)-induced infectious PTB mice model, accompanied by the increase of NF-κB, IL-6, and TNF-α (P < 0.05). Luciferase reporter gene assays showed that NF-κB was a validated target of miR-21. Furthermore, cell transfection experiments showed that miR-21 overexpression significantly decreased NF-κB mRNA expression compared with the miR-control group and blank group. Conversely, miR-21 inhibitor can enhance NF-κB mRNA expression. After the treatment of miR-21 mimics, miR-21 expression was obviously increased compared with the LPS group, accompanied by the decrease of NF-κB, TNF-α, and IL-6 mRNA expression (P < 0.05). What's more, miR-21 expression was negatively correlated with NF-κB (r=-0.87, P < 0.01). Overall, the study findings indicate that miR-21 may contribute to the pathogenesis of infection-induced PTB by upregulating the target NF-κB and that miR-21 may be a new potential therapeutic target for infection-induced PTB.