ArticleHypertension (Dallas, Tex. : 1979)2024
Differential 5'-tRNA Fragment Expression in Circulating Preeclampsia Syncytiotrophoblast Vesicles Drives Macrophage Inflammation.
Article in Hypertension (Dallas, Tex. : 1979), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed.
- Comparative Analysis of Reported Gene Targets and Binding Regions of Glu-CTC tRNA Fragments Across Human Diseases.Biomolecules · 2026Article
- Transfer RNA-derived small RNAs in female reproductive disorders: emerging roles and clinical implications.Journal of assisted reproduction and genetics · 2026Review
- New Frontiers in the Pathophysiology of Hypertensive Pregnancy Disorders: A Systematic Review of Molecular Insights into Preeclampsia.Current issues in molecular biology · 2026Review
- Several novel classes of small regulatory RNAs show widespread changes in schizophrenia and bipolar disorder and extensive linkages to critical brain processes.Translational psychiatry · 2026Article
- Article
- The role of exosomes in immunopathology and potential therapeutic implications.Cellular & molecular immunology · 2025Review
- Maternal prenatal stress induces sex-dependent changes in tRNA fragment families and cholinergic pathways in newborns.Molecular psychiatry · 2025Article
- A method to isolate syncytiotrophoblast-derived medium-large extracellular vesicle small RNA from maternal plasma.Placenta · 2025Article
- Review
- Emerging roles and therapeutic potential of tRNA-Derived small RNAs in reproductive system diseases: a review.Frontiers in cell and developmental biology · 2025Review
- Deciphering the role of tRNA-derived fragments in neurological and psychiatric disease pathogenesis.Frontiers in cellular neuroscience · 2025Review
- Article
- Extracellular Vesicles as Biomarkers of Pregnancy Complications.International journal of molecular sciences · 2024Review
- Small RNAs in the pathogenesis of preeclampsia.Placenta · 2024Review
- Placenta Extracellular Vesicles: Messengers Connecting Maternal and Fetal Systems.Biomolecules · 2024Review
- MIR193BHG inhibits the proliferation, migration and invasion of trophoblasts by upregulating p53.Experimental and therapeutic medicine · 2024Article
- Editorial: The repercussions of maternal inflammation in pre-eclampsia on fetal health and neurodevelopment.Frontiers in immunology · 2024Article
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8 authors.
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Abstract
backgroundThe relationship between placental pathology and the maternal syndrome of preeclampsia is incompletely characterized. Mismatch between placental nutrient supply and fetal demands induces stress in the syncytiotrophoblast, the layer of placenta in direct contact with maternal blood. Such stress alters the content and increases the release of syncytiotrophoblast extracellular vesicles (STB-EVs) into the maternal circulation. We have previously shown 5'-tRNA fragments (5'-tRFs) constitute the majority of small RNA in STB-EVs in healthy pregnancy. 5'-tRFs are produced in response to stress. We hypothesized STB-EV 5'-tRF release might change in preeclampsia.
methodsWe perfused placentas from 8 women with early-onset preeclampsia and 6 controls, comparing small RNA expression in STB-EVs. We used membrane-affinity columns to isolate maternal plasma vesicles and investigate placental 5'-tRFs in vivo. We quantified 5'-tRFs from circulating STB-EVs using a placental alkaline phosphatase immunoassay. 5'-tRFs and scrambled RNA controls were added to monocyte, macrophage and endothelial cells in culture to investigate transcriptional responses.
results5'-tRFs constitute the majority of small RNA in STB-EVs from both preeclampsia and normal pregnancies. More than 900 small RNA fragments are differentially expressed in preeclampsia STB-EVs. Preeclampsia-dysregulated 5'-tRFs are detectable in maternal plasma, where we identified a placentally derived load. 5'-tRF-Glu-CTC, the most abundant preeclampsia-upregulated 5'-tRF in perfusion STB-EVs, is also increased in preeclampsia STB-EVs from maternal plasma. 5'-tRF-Glu-CTC induced inflammation in macrophages but not monocytes. The conditioned media from 5'-tRF-Glu-CTC-activated macrophages reduced eNOS (endothelial NO synthase) expression in endothelial cells.
conclusionsIncreased release of syncytiotrophoblast-derived vesicle-bound 5'-tRF-Glu-CTC contributes to preeclampsia pathophysiology.
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