ArticleEpigenetics2014
miR-34a expression, epigenetic regulation, and function in human placental diseases.
Article in Epigenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 66 citations in OpenAlex.
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- Dysregulation of microRNA (miRNA) Due to Phthalate/Phthalate Metabolite Exposure and Associated Health Effects: A Narrative Review.Journal of xenobiotics · 2025Review
- DNA methylation landscape in pregnancy-induced hypertension: progress and challenges.Reproductive biology and endocrinology : RB&E · 2024Review
- MicroRNAs in the Pathogenesis of Preeclampsia-A Case-Control In Silico Analysis.Current issues in molecular biology · 2024Article
- Dysregulation of miRNA-mRNA expression in fetal growth restriction in a caloric restricted mouse model.Scientific reports · 2024Article
- Exposure to endocrine disrupting chemicals impacts immunological and metabolic status of women during pregnancy.Molecular and cellular endocrinology · 2023Article
- miR34a-5p impedes CLOCK expression in chronodisruptive C57BL/6J mice and potentiates pro-atherogenic manifestations.PloS one · 2023Article
- Effects of human placenta cryopreservation on molecular characteristics of placental mesenchymal stromal cells.Frontiers in bioengineering and biotechnology · 2023Article
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- Dysregulated miRNAs in Progression and Pathogenesis of Alzheimer's Disease.Molecular neurobiology · 2022Review
- Prenatal transcript levels and metabolomics analyses reveal metabolic changes associated with intrauterine growth restriction and sex.Open biology · 2022Article
- Characterization of Epigenetic and Molecular Factors in Endometrium of Females with Infertility.Biomedicines · 2022Article
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- Western diet-induced shifts in the maternal microbiome are associated with altered microRNA expression in baboon placenta and fetal liver.Frontiers in clinical diabetes and healthcare · 2022Article
- MicroRNA-34a: the bad guy in age-related vascular diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Epigenetic processes during preeclampsia and effects on fetal development and chronic health.Clinical science (London, England : 1979) · 2021Review
- Serum from patients with hypertension promotes endothelial dysfunction to induce trophoblast invasion through the miR‑27b‑3p/ATPase plasma membrane CaMolecular medicine reports · 2021Article
- Global miRNA/proteomic analyses identify miRNAs at 14q32 and 3p21, which contribute to features of chronic iron-exposed fallopian tube epithelial cells.Scientific reports · 2021Article
- Preeclamptic Women Have Disrupted Placental microRNA Expression at the Time of Preeclampsia Diagnosis: Meta-Analysis.Frontiers in bioengineering and biotechnology · 2021Review
- Molecular therapies delaying cardiovascular aging: disease- or health-oriented approaches.Vascular biology (Bristol, England) · 2020Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preeclampsia (PE) is the major pregnancy-induced hypertensive disorder responsible for maternal and fetal morbidity and mortality that can be associated with intrauterine growth restriction (IUGR). PE and IUGR are thought to be due to a placental defect, occurring early during pregnancy. Several placental microRNAs (miRNAs) have been shown to be deregulated in the context of placental diseases and could thus play a role in the pathophysiology of PE. Here, we show that pri-miR-34a is overexpressed in preeclamptic placentas and that its placental expression is much higher during the first trimester of pregnancy than at term, suggesting a possible developmental role. We explored pri-miR-34a regulation and showed that P53, a known activator of miR-34a, is reduced in all pathological placentas and that hypoxia can induce pri-miR-34a expression in JEG-3 cells. We also studied the methylation status of the miR-34a promoter and revealed hypomethylation in all preeclamptic placentas (associated or not with IUGR), whereas hypoxia induced a hypermethylation in JEG-3 cells at 72 h. Despite the overexpression of pri-miR-34a in preeclampsia, there was a striking decrease of the mature miR-34a in this condition, suggesting preeclampsia-driven alteration of pri-miR-34a maturation. SERPINA3, a protease inhibitor involved in placental diseases, is elevated in IUGR and PE. We show here that miR-34a overexpression in JEG-3 downregulates SERPINA3. The low level of mature miR-34a could thus be an important mechanism contributing to SERPINA3 upregulation in placental diseases. Overall, our results support a role for miR-34a in the pathophysiology of preeclampsia, through deregulation of the pri-miRNA expression and its altered maturation.
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Registered trials
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