ArticleMolecular therapy. Nucleic acids2020
miR-18a Contributes to Preeclampsia by Downregulating Smad2 (Full Length) and Reducing TGF-β Signaling.
Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Changes in microRNA expression associated with preeclampsia: a systematic review.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025Pooled it
- MicroRNA-Mediated Placental Maladaptation in Preeclampsia Pathogenesis.FASEB bioAdvances · 2026Review
- Increased TGF-β/Activin-Smad2 signaling is associated with pancreatic β-cell dysfunction and glucose intolerance in gestational diabetes mellitus.Molecular metabolism · 2026Article
- Trophoblast Function in Preeclampsia: Decoding the Mechanistic Roles of Coding and Non-Coding Genes.International journal of molecular sciences · 2025Review
- Genome-wide profiling of circulating microRNAs in adolescent idiopathic scoliosis and their relation to spinal deformity severity, and disease pathophysiology.Scientific reports · 2025Article
- Altered microRNA composition in the uterine lumen fluid in cattle (Bos taurus) pregnancies initiated by artificial insemination or transfer of an in vitro produced embryo.Journal of animal science and biotechnology · 2024Article
- Article
- Exosomal encapsulation of miR-3198 promotes proliferation and migration of trophoblasts in preeclampsia.Journal of assisted reproduction and genetics · 2024Article
- Basic Research Advances in China on Embryo Implantation, Placentation, and Parturition.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2024Article
- Holistic expression of miR-17-92 cluster in obesity, kidney diseases, cardiovascular diseases, and diabetes.Molecular biology reports · 2023Review
- miR-101-5p suppresses trophoblast cell migration and invasion via modulating the DUSP6-ERK1/2 axis in preeclampsia.Journal of assisted reproduction and genetics · 2023Article
- miR-4443/MMP2 suppresses the migration and invasion of trophoblasts through the HB-EGF/EGFR pathway in preeclampsia.Cell cycle (Georgetown, Tex.) · 2022Article
- TGF-β1/Smad3 upregulates UCA1 to promote liver fibrosis through DKK1 and miR18a.Journal of molecular medicine (Berlin, Germany) · 2022Article
- miR-218-5p Induces Interleukin-1β and Endovascular Trophoblast Differentiation by Targeting the Transforming Growth Factor β-SMAD2 Pathway.Frontiers in endocrinology · 2022Article
- Extracellular vesicles in reproduction and pregnancy.Extracellular vesicles and circulating nucleic acids · 2022Review
- Review
- Circ-PNPT1 contributes to gestational diabetes mellitus (GDM) by regulating the function of trophoblast cells through miR-889-3p/PAK1 axis.Diabetology & metabolic syndrome · 2021Article
- Placenta-Derived MicroRNAs in the Pathophysiology of Human Pregnancy.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The study investigated the regulation of Smad2 by miR-18a and its role in preeclampsia (PE). Bioinformatics analysis showed that both Smad2 and Smad3 were the predicted targets for miR-18a. Mass spectrum analysis showed that two mature Smad2 isoforms existed in human placenta: full length, Smad2(FL), and that lacking exon3, Smad2(Δexon3). The protein level of Smad2(FL), but not Smad2(Δexon3) or Smad3, was significantly increased in severe PE (sPE) placenta, which was inversely correlated with the level of miR-18a. Elevated Smad2(FL) phosphorylation level appeared in sPE placenta, and Smad2 was colocalized with miR-18a in various subtypes of trophoblasts in human placenta. Smad2(FL) was validated as the direct target of miR-18a in HTR8/SVneo cells. miR-18a enhanced trophoblast cell invasion, which was blocked by the overexpression of Smad2(FL). Furthermore, overexpression of miR-18a repressed Smad2 activation and the inhibition of trophoblast cell invasion by transforming growth factor-β (TGF-β). In conclusion, our results suggest that miR-18a inhibits the expression of Smad2(FL), but not Smad2(Δexon3) or Smad3, which can reduce TGF-β signaling, leading to the enhancement of trophoblast cell invasion. A lack of miR-18a, which results in the upregulation of Smad2(FL), contributes to the development of PE.
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