ArticleAmerican journal of reproductive immunology (New York, N.Y. : 1989)2021
Increased cell-free fetal DNA release after apoptosis and sterile inflammation in human trophoblast cells.
Article in American journal of reproductive immunology (New York, N.Y. : 1989), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Fetal-Fetal and Fetal-Maternal Microchimerism: Insights from Mammalian Placental Biology.Journal of developmental biology · 2026Review
- Association of Increased Fetal Fraction with Birthweight Discordance and Selective Fetal Growth Restriction: A Retrospective Study.International journal of women's health · 2026Article
- Analysis of prenatal diagnosis and pregnancy outcomes for rare autosomal trisomies detected by non-invasive prenatal testing in 33,079 cases.BMC medical genomics · 2025Article
- Cell-free placental DNA: What do we really know?PLoS genetics · 2024Review
- Maternal SARS-CoV-2 infection in pregnancy disrupts gene expression in Hofbauer cells with limited impact on cytotrophoblasts.PLoS pathogens · 2024Article
- Association between cell-free DNA fetal fraction and pregnant character: a retrospective cohort study of 27,793 maternal plasmas.Scientific reports · 2023Article
- Fetal DNA Causes Sex-Specific Inflammation From Human Fetal Membranes.Frontiers in physiology · 2022Article
- Maternal Monocytes Respond to Cell-Free Fetal DNA and Initiate Key Processes of Human Parturition.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
problemCell-free fetal DNA (cffDNA) shed from the placenta can be detected in maternal blood and increases incrementally during gestation. Concentrations are further elevated with pregnancy complications. Specific activators of cffDNA release in such complications have not been identified. Here, we use trophoblast cells from early and term placenta to examine cffDNA release following apoptosis, infection, and sterile inflammatory stress. METHOD OF STUDY: HTR8/SVneo cells were used to model first-trimester trophoblasts, and term cytotrophoblasts (CTBs) were isolated from placentae collected after uncomplicated deliveries. Trophoblasts were treated with varying concentrations of doxorubicin (DOX), lipopolysaccharide (LPS), or high-mobility group box protein 1 (HMGB1) for 18 h. Cells or supernatants were quantified for caspase-3/7 cleavage, pro-inflammatory cytokine secretion, and cffDNA release.
resultsBoth HTR8/SVneo and CTBs underwent caspase-3/7 cleavage following DOX treatment, with HTR8/SVneo cells more sensitive to apoptosis than term CTBs. Apoptotic cells released more cffDNA in a dose-dependent manner. Treatment with LPS resulted in an increase in pro-inflammatory IL-6 release, particularly in term CTBs compared to early trophoblasts; however, LPS did not affect cffDNA release. Lastly, while neither cell released more TNF-α following stimulation with HMGB1, both HTR8/SVneo and CTBs released significantly more cffDNA in the presence of HMGB1.
conclusionsThese data show that apoptosis and sterile inflammation induced by DOX and HMGB1, respectively, cause an increase in cffDNA concentrations in both first-trimester and term trophoblasts. Understanding physiologic release of cffDNA during healthy and complicated pregnancy can identify new targets for the diagnosis and treatment of gestational complications.
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