ArticleScientific reports2017
Antiphospholipid antibodies increase the levels of mitochondrial DNA in placental extracellular vesicles: Alarmin-g for preeclampsia.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 56 citations in OpenAlex.
- Advantages, limitations, and innovative considerations for established and emerging models of human placental syncytiotrophoblast.Human reproduction update · 2026Review
- Therapeutic and diagnostic potential of extracellular vesicle (EV)-mediated intercellular transfer of mitochondria and mitochondrial components.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Deciphering the Molecular Dialogue: Mitochondria, Epigenetics, and Extracellular Vesicles in Placental Function and Pregnancy Complications.Comprehensive Physiology · 2025Review
- Epigenetic Biomarkers in Thrombophilia-Related Pregnancy Complications: Mechanisms, Diagnostic Potential, and Therapeutic Implications: A Narrative Review.International journal of molecular sciences · 2024Review
- Machine learning: a new era for cardiovascular pregnancy physiology and cardio-obstetrics research.American journal of physiology. Heart and circulatory physiology · 2024Review
- Oxidative stress induces release of mitochondrial DNA into the extracellular space in human placental villous trophoblast BeWo cells.American journal of physiology. Cell physiology · 2024Article
- Understanding the Pathophysiology of Preeclampsia: Exploring the Role of Antiphospholipid Antibodies and Future Directions.Journal of clinical medicine · 2024Review
- Cargo exchange between human and bacterial extracellular vesicles in gestational tissues: a new paradigm in communication and immune development.Extracellular vesicles and circulating nucleic acids · 2024Review
- The pathogenesis of obstetric APS: a 2023 update.Clinical immunology (Orlando, Fla.) · 2023Review
- Early prediction of pre-eclampsia using circulating placental exosomes: Newer insights.The Indian journal of medical research · 2023Review
- Studying exogenous extracellular vesicle biodistribution by in vivo fluorescence microscopy.Disease models & mechanisms · 2023Review
- Antiphospholipid Syndrome in Pregnancy: New and Old Pathogenetic Mechanisms.International journal of molecular sciences · 2023Review
- Defining Optimal Conditions for Tumor Extracellular Vesicle DNA Extraction for Mutation Profiling.Cancers · 2022Article
- Extracellular vesicles and immune response during pregnancy: A balancing act.Immunological reviews · 2022Review
- Mitochondrial Dysfunction in the Pathogenesis of Preeclampsia.Current hypertension reports · 2022Review
- Review
- Extracellular Vesicles and Antiphospholipid Syndrome: State-of-the-Art and Future Challenges.International journal of molecular sciences · 2021Review
- Extracellular Vesicles and Preeclampsia: Current Knowledge and Future Research Directions.Sub-cellular biochemistry · 2021Review
- Antiphospholipid syndrome.Translational research : the journal of laboratory and clinical medicine · 2020Review
- Hypoxia-induced small extracellular vesicle proteins regulate proinflammatory cytokines and systemic blood pressure in pregnant rats.Clinical science (London, England : 1979) · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of preeclampsia remains unclear but placental factors are known to play a crucial role causing maternal endothelial cell dysfunction. One potential factor is placental micro- and nano- vesicles. Antiphospholipid antibodies (aPL) increase the risk of preeclampsia ten-fold, in part by damaging the mitochondria in the syncytiotrophoblast. Since mitochondrial DNA (mtDNA) is a danger- associated molecular pattern (DAMP/alarmin) that may activate endothelial cells, the aims of the current study were to investigate whether aPL affect the number of placental vesicles extruded, their mtDNA content and their ability to activate endothelial cells. Exposure of first trimester human placental explants to aPL affected neither the number nor size of extruded micro- and nano- vesicles (n = 5), however their levels of mtDNA were increased (n = 6). These vesicles significantly activated endothelial cells (n = 5), which was prevented by blocking toll-like receptor 9 (TLR-9), a receptor for extracellular DNA. Thus, aPL may increase the risk of preeclampsia in part by increasing the amount of mtDNA associated with placental vesicles. That mitochondrial DNA is recognised as a DAMP by TLR-9 to cause endothelial cell activation, raises the possibility that placental vesicles or TLR-9 might be a target for pharmaceutical intervention to reduce the consequences of aPL in pregnancy.
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