ArticleCell communication and signaling : CCS2023
Preeclampsia impedes foetal kidney development by delivering placenta-derived exosomes to glomerular endothelial cells.
Article in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Extracellular vesicle-derived TMEM106A participated in podocyte injury via EGR1 in preeclampsia.Cellular and molecular life sciences : CMLS · 2026Article
- Proteomic Epithelial-To-Mesenchymal Transition Signature in Fetoplacental Small Extracellular Vesicles of Early-Onset Preeclampsia.Journal of extracellular biology · 2026Article
- Placenta-derived extracellular vesicles in fetal health: emerging insights into brain development and environmental interactions.Experimental & molecular medicine · 2025Review
- Downregulated miR-199a-3p in Preeclamptic Placenta-derived Exosomes from Cord Blood Hinders VEGF-induced Fetal Glomerular Dysplasia Through Inhibiting Akt1(S473) Phosphorylation via Targeting PHLPP2.Stem cell reviews and reports · 2025Article
- The immune-modulatory dynamics of exosomes in preeclampsia.Archives of gynecology and obstetrics · 2025Review
- Newborn glomerular function and gestational particulate air pollution.EBioMedicine · 2024Article
- Placenta Extracellular Vesicles: Messengers Connecting Maternal and Fetal Systems.Biomolecules · 2024Review
- Correction: Preeclampsia impedes foetal kidney development by delivering placenta-derived exosomes to glomerular endothelial cells.Cell communication and signaling : CCS · 2024Article
- Attempts to preserve and visualize protein corona on the surface of biological nanoparticles in blood serum using photomodification.Beilstein journal of nanotechnology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFoetal renal dysplasia is still the main cause of adult renal disease. Placenta-derived exosomes are an important communication tool, and they may play an important role in placental (both foetal and maternal) function. We hypothesize that in women with preeclampsia, foetal renal dysplasia is impeded by delivering placenta-derived exosomes to glomerular endothelial cells.
methodsIn the present study, we established a PE trophoblast oxidative stress model to isolate exosomes from supernatants by ultracentrifugation (NO-exo and H/R-exo) and collected normal and PE umbilical cord blood plasma to isolate exosomes by ultracentrifugation combined with sucrose density gradient centrifugation (N-exo and PE-exo), then we investigated their effects on foetal kidney development by in vitro, ex vivo and in vivo models.
resultsThe PE trophoblast oxidative stress model was established successfully. After that, in in vitro studies, we found that H/R-exo and PE-exo could adversely affect glomerular endothelial cell proliferation, tubular formation, migration, and barrier functions. In ex vivo studies, H/R-exo and PE-exo both inhibited the growth and branch formation of kidney explants, along with the decrease of VE-cadherin and Occludin. In in vivo studies, we also found that H/R-exo and PE-exo could result in renal dysplasia, reduced glomerular number, and reduced barrier function in foetal mice.
conclusionsIn conclusion, we demonstrated that PE placenta-derived exosomes could lead to foetal renal dysplasia by delivering placenta-derived exosomes to foetal glomerular endothelial cells, which provides a novel understanding of the pathogenesis of foetal renal dysplasia. Video Abstract.
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