ArticleAmerican journal of physiology. Cell physiology2024
Oxidative stress induces release of mitochondrial DNA into the extracellular space in human placental villous trophoblast BeWo cells.
Article in American journal of physiology. Cell physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Review
- Acute exposure to cell-free mitochondrial DNA induces pregnancy-specific aortic endothelial dysfunction and organ-selective inflammation in rats.bioRxiv : the preprint server for biology · 2026Article
- Multi-omic profiling of early pregnancy small and large plasma extracellular vesicles reveals placental, metabolic, and structural adaptation signatures.bioRxiv : the preprint server for biology · 2026Article
- Association of Increased Fetal Fraction with Birthweight Discordance and Selective Fetal Growth Restriction: A Retrospective Study.International journal of women's health · 2026Article
- Gestational chronic intermittent hypoxia triggers maternal inflammation and disrupts placental stress responses.American journal of physiology. Cell physiology · 2025Article
- Alterations in mitochondrial DNA content in canine heart failure.BMC veterinary research · 2025Article
- IGF2BP1 Enhances Neprilysin mRNA Stability to Promote Proliferation, Invasion, and Angiogenesis in Placental Trophoblasts.International journal of general medicine · 2025Article
- The detection, biological function, and liquid biopsy application of extracellular vesicle-associated DNA.Biomarker research · 2024Review
- Machine learning: a new era for cardiovascular pregnancy physiology and cardio-obstetrics research.American journal of physiology. Heart and circulatory physiology · 2024Review
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Abstract
Circulating cell-free mitochondrial DNA (ccf-mtDNA) is an indicator of cell death, inflammation, and oxidative stress. ccf-mtDNA in pregnancies with placental dysfunction differs from that in healthy pregnancies, and the direction of this difference depends on gestational age and method of mtDNA quantification. Reactive oxygen species (ROS) trigger release of mtDNA, yet it is unknown whether trophoblast cells release mtDNA in response to oxidative stress, a common feature of pregnancies with placental pathology. We hypothesized that oxidative stress would induce cell death and release of mtDNA from trophoblast cells. BeWo cells were treated with antimycin A (10-320 µM) or rotenone (0.2-50 µM) to induce oxidative stress. A multiplex real-time quantitative PCR (qPCR) assay was used to quantify mtDNA and nuclear DNA in membrane-bound, non-membrane-bound, and vesicle-bound forms in cell culture supernatants and cell lysates. Treatment with antimycin A increased ROS (
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