ArticleEBioMedicine2018
Elevated microRNA-141-3p in placenta of non-diabetic macrosomia regulate trophoblast proliferation.
Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Discovery of placental microRNAs associated with maternal insulin sensitivity during pregnancy.Placenta · 2025Article
- The role of microRNAs in pregnancies complicated by maternal diabetes.Clinical science (London, England : 1979) · 2024Review
- The Role of Placental Non-Coding RNAs in Adverse Pregnancy Outcomes.International journal of molecular sciences · 2023Review
- Embryo cryopreservation leads to sex-specific DNA methylation perturbations in both human and mouse placentas.Human molecular genetics · 2022Article
- Downregulation of lncRNAMolecular medicine reports · 2022Article
- MiR-141-3p regulates myogenic differentiation in C2C12 myoblasts via CFL2-YAP-mediated mechanotransduction.BMB reports · 2022Article
- SP1-mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR-214-3p/MMP2 axis.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSeveral studies have reported microRNAs (miRNAs) could regulate the placental development, though the role and mechanism of miRNAs in the development of non-diabetic macrosomia (NDFMS) remains unclear.
methodsTo identify the aberrantly expressed key miRNAs in placenta of NDFMS, we employed a strategy consisting of initial screening with miRNA microarray and further validation with quantitative RT-PCR assay (qRT-PCR). In vitro cellular model and a mouse pregnancy model were used to delineate the functional effects of key miRNA on proliferation, invasion, and migration.
findingsmiR-141-3p was identified as the key miRNA with expression level significantly higher in placentas of NDFMS compared with those from normal controls. Overexpressed miR-141-3p in HTR-8/SVneo cells contributed to increased cell proliferation, invasion, and migration. miR-141-3p inhibition in HTR-8/SVneo cells resulted in decreased cell proliferation and invasion. Significantly increased infant birth weight was observed in late pregnancy of C57BL/6J mice treated with miR-141-3p agomir. However, no significant difference was found in early pregnancy of C57BL/6J mice treated with miR-141-3p agomir.
interpretationmiR-141-3p could stimulate placental cell proliferation to participate in the occurrence and development of NDFMS.
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Registered trials
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