ArticleMolecular medicine reports2020
MicroRNA‑491‑5p inhibits trophoblast cell migration and invasion through targeting matrix metalloproteinase‑9 in preeclampsia.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- MicroRNA-Mediated Placental Maladaptation in Preeclampsia Pathogenesis.FASEB bioAdvances · 2026Review
- Behind the Curtain of Abnormal Placentation in Pre-Eclampsia: From Molecular Mechanisms to Histological Hallmarks.International journal of molecular sciences · 2024Review
- Expression profiles of MMP-9 and EMMPRIN in chronic rhinosinusitis with nasal polyps.Acta otorhinolaryngologica Italica : organo ufficiale della Societa italiana di otorinolaringologia e chirurgia cervico-facciale · 2023Article
- Analysis of Varying MicroRNAs as a Novel Biomarker for Early Diagnosis of Preeclampsia: A Scoping Systematic Review of the Observational Study.International journal of preventive medicine · 2023Article
- Abnormal expression ofPeerJ · 2023Article
- MiR-200b-3p is upregulated in the placental tissues from patients with preeclampsia and promotes the development of preeclampsia via targeting profilin 2.Cell cycle (Georgetown, Tex.) · 2022Article
- Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment.International journal of molecular sciences · 2020Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insufficient invasion of trophoblasts is correlated with the development of preeclampsia (PE). MicroRNA (miR)‑491‑5p has been reported to be implicated in human cancer cell invasion; however, whether miR‑491‑5p is involved in the development of PE remains largely unclear. The aim of the present study was to investigate the role of miR‑491‑5p in trophoblastic invasion in vitro and to determine its underlying mechanism of action. The expression levels of miR‑491‑5p were validated using reverse transcription‑quantitative PCR. The effects of miR‑491‑5p on trophoblast cell invasion were evaluated in vitro. Then, the association between miR‑491‑5p and its downstream target was investigated in both cell lines and clinical specimens. miR‑491‑5p expression levels were observed to be significantly increased in the placental tissues from patients with PE. The invasive capacity of HTR‑8/SVneo trophoblast cells was suppressed following the upregulation of miR‑491‑5p and increased following the inhibition of miR‑491‑5p. Matrix metalloproteinase‑9 (MMP‑9), a well‑known regulator of trophoblast cell invasion, was discovered to be a direct target of miR‑491‑5p in HTR‑8/SVneo trophoblast cells. Moreover, miR‑491‑5p expression levels were found to be inversely correlated with MMP‑9 expression levels in placental tissues from patients with PE. The overexpression of MMP‑9 partly attenuated the inhibitory effects of miR‑491‑5p on HTR‑8/SVneo trophoblast cells invasion. Collectively, these findings suggested that the aberrant expression of miR‑491‑5p may contribute to PE through suppressing trophoblast invasion, thus highlighting the novel roles of miR‑491‑5p in the molecular pathogenesis of PE. The present study also showed that the miR‑491‑5p/MMP‑9 axis may be an effective biomarker or a viable drug target for therapeutic intervention in PE.
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