ArticlePeerJ2025
miR-381-3p contribution in mouse spontaneous abortion
Article in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Background: Recurrent spontaneous abortion (RSA) affects 1-5% of pregnant women; however, the mechanisms underlying this condition remain unknown. Dysangiogenesis in the placenta is an essential factor in the pathogenesis of RSA. Studies have verified that microRNAs (miRNAs) are vital for RSA; however, their mechanism of action in regulating angiogenesis remains unclear. Therefore, we explored the contribution of key miRNAs that regulate angiogenesis in RSA. Methods: The abortion mouse model was constructed by intraperitoneal injection of beta2-Glycoprotein I (β2-GPI). The abnormal expression of miRNAs in the placenta of the abortion mice was screened using miRNA-seq. Based on miRNA databases, miR-381-3p, which is highly expressed in abortion mice, may bind to vascular endothelial growth factor A (VEGFA). Subsequently, we investigated the effects of the miR-381-3p/VEGFA axis on the angiogenesis of vascular endothelial cells using real-time quantitative polymerase chain reaction, Transwell, wound healing, tube formation, western blotting, and dual-luciferase reporter system. Furthermore, an Results: miR-381-3p overexpression inhibited the migration and angiogenesis of C166 cells (a mouse vascular endothelial cell line), whereas miR-381-3p knockdown had the opposite effect. The dual-luciferase reporter system revealed that miR-381-3p bound to the VEGFA 3' UTR, and VEGFA knockdown counteracted the beneficial effect of the miR-381-3p inhibitor on angiogenesis. An Conclusion: miR-381-3p may cause insufficient placental blood flow by inhibiting the VEGFA pathway and can be used as a potential therapeutic target for RSA.
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