ArticleThe American journal of pathology2004
Secretion of tumor necrosis factor-alpha from human placental tissues induced by hypoxia-reoxygenation causes endothelial cell activation in vitro: a potential mediator of the inflammatory response in preeclampsia.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 208 citations in OpenAlex.
- Integrated molecular and histological profiling of preeclampsia suggests angiogenic dysregulation associated with maternal and fetal outcomes.Scientific reports · 2026Article
- Aberrant Uteroplacental and Vascular Signaling and Remodeling by Matrix Metalloproteinases in Pregnancy-Related Hypertension and Preeclampsia.Biomolecules · 2026Review
- Hydrogen sulfide modulates gene networks in hypoxia/reoxygenation-stressed trophoblasts: insights from transcriptome profiling.Frontiers in bioinformatics · 2026Article
- Late vs. Early Preeclampsia.International journal of molecular sciences · 2025Review
- Single-cell analysis of uterine artery endothelial cells reveals cytokine-induced emergence of specific immunomodulatory subtypes: implications for preeclampsia.Journal of molecular endocrinology · 2025Article
- Early prediction of preeclampsia from clinical, multi-omics and laboratory data using random forest model.BMC pregnancy and childbirth · 2025Article
- Obstructive Sleep Apnea-Associated Intermittent Hypoxia-Induced Immune Responses in Males, Pregnancies, and Offspring.International journal of molecular sciences · 2024Review
- Gut microbiota interacting with vitamin D but not anandamide might contribute to the pathogenesis of preeclampsia: a preliminary study.Frontiers in cellular and infection microbiology · 2024Article
- MicroRNA-29 differentially mediates preeclampsia-dysregulated cellular responses to cytokines in female and male fetal endothelial cells.The Journal of physiology · 2023Article
- The causal role of intestinal microbiome in development of pre-eclampsia.Functional & integrative genomics · 2023Article
- Impact of Adverse Gestational Milieu on Maternal Cardiovascular Health.Endocrinology · 2023Review
- The potential role of ischaemia-reperfusion injury in chronic, relapsing diseases such as rheumatoid arthritis, Long COVID, and ME/CFS: evidence, mechanisms, and therapeutic implications.The Biochemical journal · 2022Review
- Dissecting the Roles of Lipids in Preeclampsia.Metabolites · 2022Review
- PSG7 and 9 (Pregnancy-Specific β-1 Glycoproteins 7 and 9): Novel Biomarkers for Preeclampsia.Journal of the American Heart Association · 2022Article
- Tumor Necrosis Factor-α Induces a Preeclamptic-like Phenotype in Placental Villi via Sphingosine Kinase 1 Activation.International journal of molecular sciences · 2022Article
- Impact of offspring endothelial function fromFrontiers in surgery · 2022Review
- The First-Trimester Gestational Weight Gain Associated WithFrontiers in nutrition · 2022Article
- Uteroplacental Circulation in Normal Pregnancy and Preeclampsia: Functional Adaptation and Maladaptation.International journal of molecular sciences · 2021Review
- Histologic Chorioamnionitis in Pregnancies Complicated by Preeclampsia and the Effect on Neonatal Outcomes.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Preeclampsia and Neurodevelopmental Outcomes: Potential Pathogenic Roles for Inflammation and Oxidative Stress?Molecular neurobiology · 2021Review
21 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Preeclampsia is a hypertensive complication of human pregnancy characterized by generalized maternal endothelial cell activation. Circulating pro-inflammatory cytokines derived from the placenta are thought to play a key role. We recently demonstrated that hypoxia-reoxygenation (H/R) of placental tissues in vitro causes equivalent oxidative stress to that seen in preeclampsia. Our aim was to determine whether H/R also increases production of tumor necrosis factor-alpha (TNF-alpha), and whether conditioned media from samples exposed to H/R causes activation of human umbilical vein endothelial cells (HUVECs). Concentrations of mRNA encoding TNF-alpha were significantly higher in placental tissues subjected to H/R compared to hypoxic or normoxic controls. Although there was no difference in the concentrations of TNF-alpha protein in tissue homogenates, levels of TNF-alpha protein in the medium were significantly higher after H/R compared to controls, indicating increased secretion. Furthermore, conditioned medium from samples subjected to H/R caused increased expression of E-selectin by HUVECs, and the addition of anti-TNF-alpha antibodies significantly reduced that activation. These results are consistent with our hypothesis that intermittent perfusion of the placenta, secondary to reduced trophoblast invasion, causes increased secretion of TNF-alpha, and that this contributes to the activation of maternal endothelial cells that characterizes preeclampsia.
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