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miR-372-3p promotes preeclampsia progression by regulating twist1

Preeclampsia (PE) is a common pregnancy-related disorder worldwide. PE is mainly characterized by the defective migration and invasion of trophoblast cells. MicroRNAs (miRs) have been reported to serve an important role in PE. The purpose of the study was to explore the pathogenesis and therapeutic...

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Detalles Bibliográficos
Autores principales: Li, Ziwei, Wang, Jie, Li, Dianting, Chen, Haiying, Meng, Tao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9834874/
https://www.ncbi.nlm.nih.gov/pubmed/36686218
http://dx.doi.org/10.3892/etm.2022.11659
Descripción
Sumario:Preeclampsia (PE) is a common pregnancy-related disorder worldwide. PE is mainly characterized by the defective migration and invasion of trophoblast cells. MicroRNAs (miRs) have been reported to serve an important role in PE. The purpose of the study was to explore the pathogenesis and therapeutic targets of preeclampsia. In the present study, reverse transcription-quantitative PCR analysis revealed that the expression levels of miR-372-3p were upregulated in placental tissues from patients with PE. Notably, the expression levels of miR-372-3p were significantly upregulated in patients with early-onset PE compared with patients with late-onset PE. Moreover, in vitro analysis using wound healing, Transwell and western blotting assays demonstrated that miR-372-3p overexpression inhibited the migration, invasion and epithelial-mesenchymal transition (EMT) of HTR-8/SVneo trophoblast cells, respectively. Bioinformatics analysis and a dual luciferase reporter assay revealed that miR-372-3p is sponged by twist family bHLH transcription factor 1 (twist1). Rescue experiments found that miR-372-3p overexpression suppressed trophoblast cell migration, invasion and EMT by downregulating the expression of twist1. In conclusion, the present study revealed that high level of miR-372-3p may act as a factor to cause PE and may also be a potential novel therapeutic target for PE.